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At least 721 records · Page 40Linked to original sources
PubMed2003

Syndecan-1 transmembrane and extracellular domains have unique and distinct roles in cell spreading.

Raji cells expressing syndecan-1 (Raji-S1) adhere and spread when plated on heparan sulfate-binding extracellular matrix ligands or monoclonal antibody 281.2, an antibody directed against the syndecan-1 extracellular domain. Cells plated on monoclonal antibody 281.2 initially extend a broad lamellipodium, a response accompanied by membrane ruffling at the cell margin. Membrane ruffling then becomes polarized, leading to an elongated cell morphology. Previous work demonstrated that the syndecan-1 cytoplasmic domain is not required for these activities, suggesting important roles for the syndecan-1 transmembrane and/or extracellular domains in the assembly of a signaling complex necessary for spreading. Work described here demonstrates that truncation of the syndecan-1 extracellular domain does not affect the initial lamellipodial extension in the Raji-S1 cells but does inhibit the active membrane ruffling that is necessary for cell polarization. Replacement of the entire syndecan-1 transmembrane domain with leucine residues completely blocks the cell spreading. These data demonstrate that the syndecan-1 transmembrane and extracellular domains have important but distinct roles in Raji-S1 cell spreading; the extracellular domain mediates an interaction that is necessary for dynamic cytoskeletal rearrangements whereas an interaction of the transmembrane domain is required for the initial spreading response.

Cell Adhesion↗
PubMed2005

Actopaxin interacts with TESK1 to regulate cell spreading on fibronectin.

The focal adhesion protein actopaxin contributes to integrin-actin associations and is involved in cell adhesion, spreading, and motility. Herein, we identify and characterize an association between actopaxin and the serine/threonine kinase testicular protein kinase 1 (TESK1), a ubiquitously expressed protein previously reported to regulate cellular spreading and focal adhesion formation via phosphorylation of cofilin. The interaction between actopaxin and TESK1 is direct and the binding sites were mapped to the carboxyl terminus of both proteins. The association between actopaxin and TESK1 is negatively regulated by adhesion to fibronectin, and a phosphomimetic actopaxin mutant that promotes cell spreading also exhibits impaired binding to TESK1. Binding of actopaxin to TESK1 inhibits TESK1 kinase activity in vitro. Expression of the carboxyl terminus of actopaxin has previously been reported to retard cell spreading. This effect was reversed following overexpression of TESK1 and was found to be dependent on an inability of actopaxin carboxyl terminus expressing cells to promote cofilin phosphorylation upon matrix adhesion and caused by retention of TESK1 by this actopaxin mutant. Thus, the association between actopaxin and TESK1, which is likely regulated by phosphorylation of actopaxin, regulates TESK1 activity and subsequent cellular spreading on fibronectin.

Actin Depolymerizing Factors↗
PubMed1993

Synchrony of cell spreading and contraction force as phagocytes engulf large pathogens.

A simple micromechanical method has been used to directly measure the force of contraction in single mammalian phagocytes (blood granulocytes) during engulfment of large yeast pathogens. Both the time course of cell spreading over the yeast particle and increase in cell body contractile force were quantitated at three temperatures in the range of 23-35 degrees C. The surprising feature of the phagocyte response was that engulfment and cell body contraction occurred in a serial sequence: i.e., the phagocyte spread rapidly over the particle at a steady rate with no detectable cell body contraction; when spreading stopped, contraction force in the cell body then rose steadily to a plateau level that remained stationary until the next sequence of spreading and contraction. Both spreading and contraction exhibited abrupt start/stop kinetics. Also impressive, the cell contraction force stimulated by phagocytosis was quite large (approximately 10(-8) N)-two orders of magnitude larger than the force necessary to deform passive phagocytes to the same extent. If distributed uniformly over the cell cross section, the contraction force is equivalent to an average contractile stress of approximately 10(3) N/m2 (0.01 Atm). These physical measurements in situ set critical requirements for the mechanism of force generation in granulocytes, imply that a major increase in network cross-linking accompanies build-up in contractile force and that subsequent network dissolution is necessary for locomotion.

Biomechanical Phenomena↗
PubMed1981

Studies on cell adhesion and recognition. II. The kinetics of cell adhesion and cell spreading on surfaces coated with carbohydrate-reactive proteins (glycosidases and lectins) and fibronectin.

The kinetics of cell attachment and cell spreading on the coated surfaces of two classes of carbohydrate-reactive proteins, enzymes and lectins, have been compared with those on fibronectin-coated surfaces with the following results: (a) A remarkable similarity between the kinetics of cell attachment to fibronectin-coated and glycosidase-coated surfaces was found. In contrast, cell attachment kinetics induced by lectin- and galactose oxidase-coated surfaces, in general, were strikingly different from those on fibronectin and glycosidase surfaces. The distinction between fibronectin- or glycosidase- and lectin- or galactose oxidase (an enzyme with lectin-type characteristics)-coated surfaces was further supported by the finding that cytochalasin B and EDTA inhibited cell attachment to fibronectin- and glycosidase-coated surfaces but not lectin-coated surfaces. (b) Fibronectin, if labeled and added to a cell suspension, showed only low or negligible interaction with the cell surface. However, fibronectin absorbed on plastic surfaces showed a high cell-attaching activity. It is assumed that fibronectin coated on plastic surfaces may form polyvalent attachment sites in contrast to its lower valency in aqueous solution. (c) Various inhibitors of cell attachment to both fibronectin-, galactose oxidase-, and lectin-coated surfaces were effective only during the first few minutes of the adhesion assay, after which time the attached cells became insensitive to the inhibitors. It is suggested that the initial specific recognition on either lectin-type or fibronectin-type surfaces is followed by an active cell-dependent attachment process. The primary role of the adhesion surface is to stimulate the cell-dependent attachment response. (d) Cells attached on tetravalent concanavalin A (Con A) spread very rapidly and quantitatively, whereas divalent succinyl Con A and monovalent Con A were effective stimulators of cell attachment but not cell spreading. Cross-linking of succinyl Con A restored the cell spreading activity. Tetravalent Con A surfaces specifically bind soluble glycoproteins, whereas succinyl Con A has a greatly reduced ability to bind the same glycoproteins. These results suggest that cross-linking of cell surface glycoproteins by the multivalent adhesive surface may trigger the cellular reaction leading to cell spreading.

Animals↗
PubMed1982

Cytostructural dynamics of spreading and translocating cells.

Cytostructural changes during fibroblast spreading and translocation and during the transition between the two states have been studied in living cells and in the same cells after fixation and immunofluorescent staining. In time-lapse sequences we observe that birefringent arcs, sometimes circles, concentric with the cell perimeter, form near the periphery of a spreading cell, or that arcs form near the leading edge of a locomoting cell. The arcs move toward the nucleus, where they disappear. In spreading cells, radial stress fibers extend from the region of the cell nucleus to the periphery. The arcs or circles and the stress fibers are visualized in the same cells after fixation and staining with fluorescein-conjugated antiactin antibodies. Stained images of spreading cells show the arcs and stress fibers in the same plane of focus. At points of intersection with arcs, stress fibers are bent toward the substrate on which the cell is moving. During a transitional stage between spreading and translocation the cytostructure undergoes reproducible changes. Arcs and circle cease to form. The radial stress fibers elongate, spiral around the nucleus, and move to the periphery as a band of filaments. We interpret the moving arcs as condensations of a microfilament network that move toward the nucleus as compression waves. As elements of the net are brought close together by the compression wave, contraction may occur and facilitate the condensations.

Actins↗
PubMed1980

Importance of antibodies to the fusion glycoprotein of paramyxoviruses in the prevention of spread of infection.

The effects of monospecific antibodies to the viral glycoprotein with hemagglutinating and neuraminidase activity (HN) and the viral glycoprotein with membrane-fusing activity (F) of the paramyxovirus simian virus 5 (SV5) on the spread of infection in two cell types have been investigated. In CV-1 cells, infection can spread by either released progeny virus adsorbing to and infecting other cells, or by fusion of an infected cell with an adjacent cell as a result of the cell-fusing activity of the F glycoprotein. In these cells, antibodies specific for the HN glycoprotein prevented the dissemination of infection by released infectious virus, but spread by cell fusion was not inhibited. Antibodies to the F glycoprotein completely prevented the spread of infection in these cells. In Madin-Darby bovine kidney cells, which are relatively resistant to SV5-induced fusion, antibodies to either the HN or F glycoproteins were capable of preventing the dissemination of infection. These results indicate that effective immunological prevention of the spread of paramyxovirus infection requires the presence of antibodies that inactivate the F glycoprotein. This requirement for anti-F antibodies has obvious implications for the design of effective paramyxovirus vaccines and provides an explanation for previous failures of formalin-inactivated paramyxovirus vaccines as well as additional insight into the possible immunopathological mechanisms involved in the atypical and severe infections that have occurred in individuals who received inactivated paramyxovirus vaccines and were subsequently infected by the virus.

Animals↗
PubMed1998

Activation of Rac and Cdc42 by integrins mediates cell spreading.

Adhesion to ECM is required for many cell functions including cytoskeletal organization, migration, and proliferation. We observed that when cells first adhere to extracellular matrix, they spread rapidly by extending filopodia-like projections and lamellipodia. These structures are similar to the Rac- and Cdc42-dependent structures observed in growth factor-stimulated cells. We therefore investigated the involvement of Rac and Cdc42 in adhesion and spreading on the ECM protein fibronectin. We found that integrin-dependent adhesion led to the rapid activation of p21-activated kinase, a downstream effector of Cdc42 and Rac, suggesting that integrins activate at least one of these GTPases. Dominant negative mutants of Rac and Cdc42 inhibit cell spreading in such a way as to suggest that integrins activate Cdc42, which leads to the subsequent activation of Rac; both GTPases then contribute to cell spreading. These results demonstrate that initial integrin-dependent activation of Rac and Cdc42 mediates cell spreading.

3T3 Cells↗
PubMed2004

Spread fortified with vitamins and minerals induces catch-up growth and eradicates severe anemia in stunted refugee children aged 3-6 y.

BACKGROUND: Multiple micronutrient deficiencies are often the basic causative factor in stunting and anemia, 2 conditions that affect entire generations of children in deprived populations. No generally accepted recommendations for micronutrient intakes for recovery from stunting are available. OBJECTIVE: The objective was to assess the effect of a highly nutrient-dense spread fortified with vitamins and minerals, with or without antiparasitic metronidazole treatment, in correcting retarded linear growth and reducing anemia in stunted children. DESIGN: Saharawi refugee children (n = 374) aged 3-6 y with initial height-for-age z scores <-2 were assigned to 1 of 5 groups: fortified spread (FS), fortified spread plus metronidazole (FS+M), unfortified spread (US), unfortified spread plus metronidazole (US+M), or control. Supervised supplementation was given daily for 6 mo. Weight, height, knee-heel length, hematologic indexes, parasitic infections, and morbidity were assessed at 0, 3, and 6 mo. RESULTS: Linear growth of children fed FS was 30% faster at 3 mo than in US and control groups, after which height-for-age z scores increased only slightly in the FS group and remained unchanged in the other groups. No additional benefits from metronidazole were observed. Increase in hemoglobin concentrations in the FS group at 6 mo was twofold that in the US and control groups (37 +/- 40, 19 +/- 15, and 16 +/- 17 g/L, respectively; P < 0.0001), and anemia was reduced by nearly 90%. CONCLUSIONS: FS, and not US, induces catch-up growth in stunted children whose diets are poor in micronutrients. Our trial provides support for delivering multiple micronutrients to reverse stunting and reduce anemia in children up to age 6 y.

Algeria↗
PubMed2006

Using data on social contacts to estimate age-specific transmission parameters for respiratory-spread infectious agents.

The estimation of transmission parameters has been problematic for diseases that rely predominantly on transmission of pathogens from person to person through small infectious droplets. Age-specific transmission parameters determine how such respiratory agents will spread among different age groups in a human population. Estimating the values of these parameters is essential in planning an effective response to potentially devastating pandemics of smallpox or influenza and in designing control strategies for diseases such as measles or mumps. In this study, the authors estimated age-specific transmission parameters by augmenting infectious disease data with auxiliary data on self-reported numbers of conversational partners per person. They show that models that use transmission parameters based on these self-reported social contacts are better able to capture the observed patterns of infection of endemically circulating mumps, as well as observed patterns of spread of pandemic influenza. The estimated age-specific transmission parameters suggested that school-aged children and young adults will experience the highest incidence of infection and will contribute most to further spread of infections during the initial phase of an emerging respiratory-spread epidemic in a completely susceptible population. These findings have important implications for controlling future outbreaks of novel respiratory-spread infectious agents.

Adolescent↗
PubMed1981

Effects of posture on the spread of isobaric and hyperbaric amethocaine.

The effects of posture on the spread of isobaric and hyperbaric amethocaine were studied after intrathecal injection in 60 patients. Gravity had no effect on the spread of isobaric solutions and, while hyperbaric solutions did spread under the effect of gravity, it was found that posture could not be used to control spread effectively. The results also show that the dose of local anaesthetic injected had a more important effect on the duration of blockade than on the spread.

Anesthesia, Spinal↗
PubMed1997

The spread of an advantageous allele across a barrier: the effects of random drift and selection against heterozygotes.

A local barrier to gene flow will delay the spread of an advantageous allele. Exact calculations for the deterministic case show that an allele that is favorable when rare is delayed very little even by a strong barrier: its spread is slowed by a time proportional to log((B/sigma) square root of 2S)/S, where B is the barrier strength, sigma the dispersal range, and fitnesses are 1:1 + S:1 + 2S. However, when there is selection against heterozygotes, such that the allele cannot increase from low frequency, a barrier can cause a much greater delay. If gene flow is reduced below a critical value, spread is entirely prevented. Stochastic simulations show that with additive selection, random drift slows down the spread of the allele, below the deterministic speed of sigma square root of 2S. The delay to the advance of an advantageous allele caused by a strong barrier can be substantially increased by random drift and increases with B/(2S rho sigma 2) in a one-dimensional habitat of density rho. However, with selection against heterozygotes, drift can facilitate the spread and can free an allele that would otherwise be trapped indefinitely by a strong barrier. We discuss the implications of these results for the evolution of chromosome rearrangements.

Alleles↗
PubMed1990

Capsaicin interferes with the centrifugal spread of virus in primary and recurrent genital herpes simplex virus infections.

The neural spread of herpes simplex virus (HSV) via sensory nerves is an essential component of disease pathogenesis. Capsaicin, a specific toxin for sensory C-type fibers, interferes with neuronal function including axonal transport. Capsaicin treatment of guinea pigs before intravaginal HSV inoculation did not prevent ganglionic infection but ameliorated cutaneous herpetic disease, suggesting that anterograde but not retrograde virus spread involved a capsaicin-sensitive process. Similarly, treatment of latently infected animals reduced both spontaneous and ultraviolet radiation-induced herpetic recurrences, suggesting that capsaicin interfered with the anterograde spread of reactivated virus. These results suggest that the centrifugal spread of virus may involve either different pathways or mechanisms than are involved in centripetal HSV spread. The use of selective neuropharmacologic agents such as capsaicin may prove useful in further defining the pathophysiology of HSV disease.

Animals↗
PubMed2004

Comparison of intraductal spread on dynamic contrast-enhanced MRI with clinicopathologic features in breast cancer.

OBJECTIVE: Contrast-enhanced magnetic resonance imaging (CE-MRI) has emerged as a new diagnostic technology in various breast cancer treatments. However, little is known about the correlation between intraductal spread on CE-MRI and clinicopathologic features. This study was designed to evaluate these correlations for the surgical planning of breast cancer. METHODS: Twenty-six breast cancer lesions (in 26 female patients) treated by breast conserving surgery between March 2001 and March 2003 were evaluated retrospectively. CE-MRI was performed with a 1.5 T unit using a dedicated bilateral breast coil. RESULTS: In detecting intraductal spread of breast cancer, the sensitivity, specificity and accuracy of CE-MRI were 82.4%, 60.0% and 77.3%, respectively. On mammography (MMG), these were 21.1%, 100.0% and 42.3%, respectively. Therefore, CE-MRI has a higher sensitivity and accuracy, although with a lower specificity than MMG. Compared with breast cancer lesions without intraductal spread on CE-MRI, lesions with intraductal spread on CE-MRI were found more frequently in larger-sized tumors (P = 0.0088). CONCLUSION: Preoperative evaluation for intraductal spread by CE-MRI should be more useful than by MMG for breast cancer. When making the surgical decision regarding excision range, particular attention should be paid to this consideration for patients with larger-sized cancer tumors.

Aged↗
PubMed2003

The impact of needle-exchange programs on the spread of HIV among injection drug users: a simulation study.

OBJECTIVE: To determine the impact of the implementation of a needle-exchange program (NEP) on the spread of human immunodeficiency virus (HIV) in an injection drug user (IDU) community. We conducted a Monte Carlo simulation study of a theoretical population of 10000 IDUs. The population was followed monthly from 1984 to 2000. HIV was assumed to be transmitted only by needle sharing. The NEP was introduced in 1989 and evaluated over a period of 11 years. The impacts of the proportion of the population attending the NEP, the risk level of IDUs attending the NEP, the reduction in needle-sharing frequency, and the number of new needle-sharing partners acquired at the NEP on prevalence and incidence of HIV were determined. Increasing the proportion of the population who always attend the NEP and eliminating needle-sharing incidents among IDUs who always attended the NEP were the most effective ways of reducing the spread of HIV. Attracting high-risk users instead of lower risk users to the NEP also reduced the spread of HIV, but to a lesser extent. NEPs are effective at reducing the spread of HIV; even under the worst case scenario of low risk users more likely to attend the NEP, one additional partner per month as a result of attending the NEP, and poor NEP attendance, the estimated prevalence was still less than that from the scenario without an NEP. Under our model, NEPs were shown to reduce the spread of HIV significantly. Efforts should be focused on getting as many IDUs as possible to become regular NEP attenders and stop sharing needles rather than partially reducing the frequency of sharing by a larger number of IDUs.

British Columbia↗
PubMed2006

The effect of silicon on the infection by and spread of Pythium aphanidermatum in single roots of tomato and bitter gourd.

The effect of silicon (Si) supply on the infection and spread of Pythium aphanidermatum was studied in the roots of tomato [Lycopersicon esculentum (=Solanum lycopersicum), an Si excluder] and bitter gourd (Mormodica charantia, an Si intermediate accumulator). Individual roots were mounted into PVC compartmented boxes which allowed the application of Si and zoospores to defined root zones. Two days after inoculation, root growth was recorded, and P. aphanidermatum colonization of individual root sections was determined by ELISA. In tomato as well as in bitter gourd the root tip was the root section most sensitive to P. aphanidermatum infection. Application of Si did not affect severe root-growth inhibition by P. aphanidermatum in either species. However, continuous Si supply significantly inhibited the basipetal spread of the pathogen from the infected root apex in bitter gourd but not in tomato. Si application to the roots only during pretreatment or only during/after the infection of the roots failed to inhibit the spread of P. aphanidermatum. Determination and compartmentation of Si in the roots of bitter gourd revealed that apoplastic Si was not, but symplastic Si was, associated with the ability of the plant to reduce the spread of the fungus in roots. It is concluded that accumulation of Si in the root cell walls does not represent a physical barrier to the spread of P. aphanidermatum in bitter gourd and tomato roots. The maintenance of elevated symplastic Si contents is a prerequisite for Si-enhanced resistance against P. aphanidermatum.

Antiparasitic Agents↗
PubMed1996

Dural puncture with a 26-gauge spinal needle affects spread of epidural anesthesia.

Combined spinal and epidural anesthesia may increase the risk of epidurally administered drugs spreading into the subarachnoid space through the dural hole. We studied the effect of dural puncture with a 26-gauge needle on the spread of analgesia induced by epidural injection of local anesthetics. Forty patients were randomly assigned to control and dural puncture groups. In the dural puncture group, the dura was punctured with a 26-gauge Whitacre spinal needle at L2-3 but no drug was injected. In both groups, an 18-gauge epidural catheter was inserted 4 cm cephalad into the epidural space at L2-3 and 15 mL of 2% mepivacaine without epinephrine was injected. Analgesia was assessed by pinprick at 5, 10, 15, and 20 min after injection and at the end of surgery. The caudal spread of analgesia was significantly greater in the dural puncture group than in the control group 15 and 20 min after injection (P < 0.01), but the cranial spread of analgesia was not different between the two groups. We conclude that dural puncture (without drugs) using a 26-gauge Whitacre spinal needle before epidural injection increases caudal spread of analgesia induced by epidural local anesthetics.

Adult↗
PubMed2001

Spreading of the tears after a blink: velocity and stabilization time in healthy eyes.

PURPOSE: To quantify the tear spreading velocity and stabilization time after blinks in healthy patients. METHODS: Video recordings (magnification, x130) were made of the movements of naturally occurring particles in the tear film while patients blinked naturally. After each blink, tear spreading velocity was computed every 40 milliseconds from particle displacements determined from a frame-by-frame analysis of the records. RESULTS: After a blink, tears moved rapidly upward over the cornea. Forty milliseconds after passage of the lid, the velocity was 7.34 +/- 2.73 mm/s (mean +/- standard deviation, n = 20). The time to tear stabilization (i.e., zero velocity) was 1.05 +/- 0.30 seconds. The decay of spreading velocity with time was well described by a logarithmic function for all individual patient data (R2 range, 0.88-0.99; n = 20). We have shown that initial velocity and stabilization time are independent descriptors of tear spreading. Meibomian gland expression markedly reduced initial velocity leaving a normal stabilization time, whereas inhalation of an irritant reduced stabilization time leaving a normal initial velocity. In a patient with Sjögren syndrome, punctal plugs rapidly restored initial velocity and stabilization time from near zero values to normal values. CONCLUSION: We provide normal values for two descriptors of tear spreading, namely initial velocity and time to stabilization. These values can be modified by manipulations that alter tear constituents. Consequently, these descriptors may provide a basis for quantitative, noninvasive tear assessment.

Adolescent↗
PubMed1998

Nitric oxide scavenging by hemoglobin or nitric oxide synthase inhibition by N-nitro-L-arginine induces cortical spreading ischemia when K+ is increased in the subarachnoid space.

We investigated the combined effect of increased brain topical K+ concentration and reduction of the nitric oxide (NO.) level caused by nitric oxide scavenging or nitric oxide synthase (NOS) inhibition on regional cerebral blood flow and subarachnoid direct current (DC) potential. Using thiopental-anesthetized male Wistar rats with a closed cranial window preparation, brain topical superfusion of a combination of the NO. scavenger hemoglobin (Hb; 2 mmol/L) and increased K+ concentration in the artificial cerebrospinal fluid ([K+]ACSF) at 35 mmol/L led to sudden spontaneous transient ischemic events with a decrease of CBF to 14+/-7% (n=4) compared with the baseline (100%). The ischemic events lasted for 53+/-17 minutes and were associated with a negative subarachnoid DC shift of -7.3+/-0.6 mV of 49+/-12 minutes' duration. The combination of the NOS inhibitor N-nitro-L-arginine (L-NA, 1 mmol/L) with [K+]ACSF at 35 mmol/L caused similar spontaneous transient ischemic events in 13 rats. When cortical spreading depression was induced by KCl at a 5-mm distance, a typical cortical spreading hyperemia (CSH) and negative DC shift were measured at the closed cranial window during brain topical superfusion with either physiologic artificial CSF (n=5), or artificial CSF containing increased [K+]ACSF at 20 mmol/L (n=4), [K+]ACSF at 3 mmol/L combined with L-NA (n=10), [K+]ACSF at 10 mmol/L combined with L-NA (five of six animals) or [K+]ACSF at 3 mmol/L combined with Hb (three of four animals). Cortical spreading depression induced longlasting transient ischemia instead of CSH, when brain was superfused with either [K+]ACSF at 20 mmol/L combined with Hb (CBF decrease to 20+/-20% duration 25+/-21 minutes, n=4), or [K+]ACSF at 20 mmol/L combined with L-NA (n=19). Transient ischemia induced by NOS inhibition and [K],ACSF at 20 mmol/L propagated at a speed of 3.4+/-0.6 mm/min, indicating cortical spreading ischemia (CSI). Although CSH did not change oxygen free radical production, as measured on-line by in vivo lucigenin-enhanced chemiluminescence, CSI resulted in the typical radical production pattern of ischemia and reperfusion suggestive of brain damage (n=4). Nimodipine (2 microg/kg body weight/min intravenously) transformed CSI back to CSH (n=4). Vehicle had no effect on CSI (n=4). Our data suggest that the combination of decreased NO. levels and increased subarachnoid K+ levels induces spreading depression with acute ischemic CBF response. Thus, a disturbed coupling of metabolism and CBF can cause ischemia. We speculate that CSI may be related to delayed ischemic deficits after subarachnoid hemorrhage, a clinical condition in which the release of Hb and K+ from erythrocytes creates a microenvironment similar to the one investigated here.

Animals↗