Biomedical subjects

C A Gleason

Publications and source records attributed to C A Gleason.

At least 19 recordsLinked to original sources

PubMed2004

The nematode-resistance gene, Mi-1, is associated with an inverted chromosomal segment in susceptible compared to resistant tomato.

The gene Mi-1 confers effective resistance in tomato ( Lycopersicon esculentum) against root-knot nematodes and some isolates of potato aphid. This locus was introgressed from L. peruvianum into the corresponding region on chromosome 6 in tomato. In nematode-resistant tomato, Mi-1 and six homologs are grouped into two clusters separated by 300 kb. Analysis of BAC clones revealed that the Mi-1 locus from susceptible tomato carried the same number and distribution of Mi-1 homologs, as did the resistant locus. Molecular markers flanking the resistant and susceptible loci were in the same relative orientation, but markers between the two clusters were in an inverse orientation. The simplest explanation for these observations is that there is an inversion between the two clusters of homologs when comparing the Mi-1 loci from L. esculentum and L. peruvianum. Such an inversion may explain previous observations of severe recombination suppression in the region. Two Mi-1 homologs identified from the BAC library derived from susceptible tomato are not linked to the chromosome 6 locus, but map to chromosome 5 in regions known to contain resistance gene loci in other solanaceous species.

Animals↗

PubMed2001

Fetal cerebral and peripheral circulatory responses to hypoxia after nitric oxide synthase inhibition.

The increase in cerebral blood flow (CBF) during hypoxia in fetal sheep at 0.6 gestation is less than the increase at 0.9 gestation when normalized for differences in baseline CBF and oxygen consumption. Nitric oxide (NO) synthase (NOS) catalytic activity increases threefold during this period of development. We tested the hypothesis that administration of the NOS inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME) decreases the CBF response to systemic hypoxia selectively at 0.9 gestation. We also tested whether any peripheral vasoconstriction during hypoxia is potentiated by L-NAME at 0.9 gestation. Administration of L-NAME increased arterial blood pressure and decreased microsphere-determined CBF during normoxia in fetal sheep at both 0.6 and 0.9 gestation. With subsequent reduction of arterial oxygen content by approximately 50%, the percent increase in forebrain CBF in a control group (57 +/- 11%; +/- SE) and L-NAME-treated group (51 +/- 6%) was similar at 0.6 gestation. Likewise, at 0.9 gestation, the increase in CBF was similar in control (90 +/- 25%) and L-NAME (80 +/- 28%) groups. At 0.9 gestation, L-NAME treatment attenuated the increase in coronary blood flow and increased gastrointestinal vascular resistance during hypoxia. We conclude that NO exerts a basal vasodilatory influence in brain as early as 0.6 gestation in fetal sheep but is not an important mechanism for hypoxic vasodilation in brain at either 0.6 or 0.9 gestation. Thus the developmental increase in NOS catalytic capacity does not appear to be responsible for developmental increases in the CBF response to hypoxia during this period. In contrast, NO modulates the vascular response to hypoxia in heart and gastrointestinal tract.

Analysis of Variance↗

PubMed2001

Blood-brain barrier permeability during dopamine-induced hypertension in fetal sheep.

Dopamine is often used as a pressor agent in sick newborn infants, but an increase in arterial blood pressure could disrupt the blood-brain barrier (BBB), especially in the preterm newborn. Using time-dated pregnant sheep, we tested the hypothesis that dopamine-induced hypertension increases fetal BBB permeability and cerebral water content. Barrier permeability was assessed in nine brain regions, including cerebral cortex, caudate, thalamus, brain stem, cerebellum, and spinal cord, by intravenous injection of the small tracer molecule [(14)C]aminoisobutyric acid at 10 min after the start of dopamine or saline infusion. We studied 23 chronically catheterized fetal sheep at 0.6 (93 days, n = 10) and 0.9 (132 days, n = 13) gestation. Intravenous infusion of dopamine increased mean arterial pressure from 38 +/- 3 to 53 +/- 5 mmHg in 93-day fetuses and from 55 +/- 5 to 77 +/- 8 mmHg in 132-day fetuses without a decrease in arterial O(2) content. These 40% increases in arterial pressure are close to the maximum hypertension reported for physiological stresses at these ages in fetal sheep. No significant increases in the brain transfer coefficient of aminoisobutyric acid were detected in any brain region in dopamine-treated fetuses compared with saline controls at 0.6 or 0.9 gestation. There was also no significant increase in cortical water content with dopamine infusion at either age. We conclude that a 40% increase in mean arterial pressure during dopamine infusion in normoxic fetal sheep does not produce substantial BBB disruption or cerebral edema even as early as 0.6 gestation.

Aminoisobutyric Acids↗

PubMed2001

Time dependent smooth muscle regeneration and maturation in a bladder acellular matrix graft: histological studies and in vivo functional evaluation.

PURPOSE: We evaluated the time dependence of smooth muscle regeneration and restoration of in vivo functional properties in bladder augmented with a bladder acellular matrix graft. MATERIALS AND METHODS: A total of 45 Sprague-Dawley rats underwent augmentation cystoplasty with a bladder acellular matrix graft. Two rats each were sacrificed at various intervals within the first 21 days and 6 each were sacrificed at 4, 8 and 12 weeks. This second group underwent preoperative and postoperative assessment of bladder function, including cystometry, electrostimulation and stimulation with ice water, potassium and carbachol, as well as labeling of the bladder wall by the injection of fluorescent microspheres. After sacrifice slides of the bladders prepared for hematoxylin and eosin, trichrome, KI67, vimentin, desmin, smooth muscle specific alpha-actin and fluorescent microspheres were evaluated. RESULTS: Within 2 weeks the number of cells in the matrix as well as the proliferation index increased rapidly and then decreased gradually. Erythrocytes and inflammatory cells were found in the matrix within 2 to 4 days, followed by fibroblasts. A bladder host-to-matrix shift was evident by the appearance of microspheres in the matrix. Cell marker expression indicated the early appearance of vimentin and alpha-actin within the first 10 days. Distinct desmin expression was observed later, when the first smooth muscle cells were recognized. Functional evaluation revealed restored bladder function at 12 weeks. CONCLUSIONS: The time dependent increase of muscle cell markers during smooth muscle cell regeneration in a bladder acellular matrix graft is concordant with the progressive restoration of bladder function. These results may support the bladder acellular matrix graft concept for clinical application.

Actins↗

PubMed2000

Comparison of cerebrovascular effects of intravenous cocaine injection in fetal, newborn, and adult sheep.

Cocaine may cause stroke, intracranial hemorrhage, seizures, and neurobehavioral abnormalities in fetuses, newborns, and adults, and there could be developmental and/or species differences in mechanisms for these cocaine-induced cerebrovascular effects. To evaluate developmental differences in responses to cocaine, we compared the cerebrovascular and metabolic responses to a 2 mg/kg iv cocaine dose in unanesthetized fetal (n = 8, previously reported, direct fetal injection), newborn (n = 6), and adult (n = 12) sheep. We measured cerebral blood flow, mean arterial blood pressure, and arterial and venous O(2) content, and we calculated cerebral O(2) consumption and cerebral vascular resistance at baseline and at 30 s and at 5, 15, and 60 min after cocaine injection. Cerebral blood flow increased 5 min after injection in the fetus and newborn, but not until 15 min in the adult. In the fetus, cocaine caused a transient cerebral vasoconstriction at 30 s; in all three groups, cocaine caused cerebral vasodilation, which was delayed in the adult. Cerebral metabolic O(2) consumption increased 5 min after injection in the fetus and newborn, but not until 15 min after injection in the adult. Arterial O(2) content decreased 5 min after injection in the fetus and 15 min after injection in the adult. We speculate that clinical differences in response to cocaine injection may be explained, in part, by these developmental differences in the cerebrovascular and metabolic responses to cocaine.

Animals↗

PubMed1999

Bladder acellular matrix graft: in vivo functional properties of the regenerated rat bladder.

The purpose of this study was to determine whether the rat urinary bladder augmented by an acellular matrix graft can restore the bladder's low-pressure reservoir function and preserve normal micturition. After partial cystectomy (> 50%) and grafting with the bladder acellular matrix graft (BAMG), storage and voiding functions were monitored in 20 rats by means of a specially designed "micturition cage," leak-point cystography, and cystometry. After 4 months, sections (n = 6) were examined histologically to evaluate regeneration of bladder wall components within the BAMG. Bladder capacity and compliance increased progressively and were significantly higher in the grafted animals than in controls (partial cystectomy only), and volumes per void were significantly higher than in either control or normal animals. At 4 months, the regenerated urothelium, smooth muscle, blood vessels and nerves within the BAMG were qualitatively identical to normal bladder wall. Augmentation cystoplasty with the homologous BAMG leads to morphologic and functional rat bladder regeneration, thus enhancing low-pressure reservoir function and preserving normal micturition.

Animals↗

PubMed1999

Skin care management practices for premature infants.

OBJECTIVE: To describe current skin care practices for preterm infants in neonatal intensive care units in the United States. We hypothesized that there would be little consensus among facilities. STUDY DESIGN: Neonatal intensive care units (n = 823) listed in the 1996 United States Neonatologists Directory (American Academy of Pediatrics, Section on Perinatal Pediatrics) were sent a 28-question survey dealing with many aspects of neonatal skin care along with descriptive data about their neonatal intensive care unit. Descriptive data analysis was performed. RESULTS: A total of 305 surveys were returned (37% return rate); of these, 241 of the respondents reported admitting infants weighing < or = 1000 gm. Some neonatal skin care practices showed wide consensus (> 70%) (e.g., scrub procedure for staff; use of a skin barrier under tapes/adhesives), whereas other practices showed little consensus (< 30%) (e.g., routine surveillance cultures; use of Aquaphor). CONCLUSION: Consensus on skin care practices was not found among neonatal intensive care units. Data from this survey can be used to develop studies to examine whether certain skin care management practices can improve neonatal outcomes.

Body Temperature Regulation↗

PubMed1999

Propranolol blocks cocaine-induced cerebral vasodilation in newborn sheep.

OBJECTIVE: The objective of this study was to test the hypothesis that cocaine-induced cerebral vasodilation in newborn sheep is mediated via beta-adrenergic receptor activation. DESIGN: The cerebral effects of a single intravenous injection of cocaine (4 mg/kg) given 30 mins after pretreatment with propranolol (1 mg/kg) were studied and compared with the results from a previous study using an identical cocaine protocol without propranolol pretreatment. SUBJECTS: Seven chronically catheterized, unanesthetized newborn sheep (6 +/- 1 days old). MEASUREMENTS: Cerebral blood flow using radiolabeled microspheres, mean arterial blood pressure (MAP), heart rate, and cerebral arterial and venous oxygen content were measured at baseline, after administration of propranolol, and 0.5, 5, 15, and 60 mins after cocaine injection. Cerebrovascular resistance was calculated as the MAP divided by the cerebral blood flow. MAIN RESULTS: Propranolol injection alone caused no systemic or cerebral physiologic changes other than an 11 +/- 2% (mean +/- SEM) decrease in heart rate, which was sustained after cocaine injection. In contrast to previous studies showing cerebral vasodilation (25% decrease in cerebrovascular resistance) and acute hypertension (57% increase in MAP) 30 secs after cocaine injection, there were no changes in cerebrovascular resistance after cocaine injection and after propranolol pretreatment and there was only a 23 +/- 7% increase in MAP 30 secs after injection, with a return to baseline by 15 mins. Cocaine and norepinephrine levels were similar to those previously reported in the newborn sheep after an injection of 4 mg/kg cocaine. CONCLUSION: Propranolol blocks cocaine-induced cerebral vasodilation and blunts the acute hypertension in newborn sheep, suggesting that cocaine's cerebrovascular effects in the developing brain are mediated, at least in part, by beta-adrenergic receptor activation.

Adrenergic beta-Antagonists↗

PubMed1998

Bladder acellular matrix graft in rats: its neurophysiologic properties and mRNA expression of growth factors TGF-alpha and TGF-beta.

To assess the neurophysiologic properties and molecular mechanisms of the bladder acellular matrix graft (BAMG), we performed cystometric and neurophysiologic studies in male Sprague-Dawley rats (n = 46) at varying intervals. The animals were assigned to 3 groups: 1) normal, 2) partial cystectomy (>50%), and 3) partial cystectomy (>50%) and grafting with a BAMG of equal size. Additionally, matrix-grafted and host bladders were processed for analysis of mRNA expression of transforming growth factor (TGF)-alpha, TGF-beta1, TGF-beta2, and TGF-beta3 by reverse transcriptase polymerase chain reaction. Matrix-grafted bladders showed a significantly higher bladder capacity at 3 and 6 weeks and 4 months than those with partial cystectomy alone, and a significantly higher bladder capacity at 4 months than in normal controls (P < or = 0.01). Residual urine volume was significantly increased at 4 months. Electrostimulation of the pelvic nerve provoked generalized bladder contractions, a response that was reduced by atropine and hexamethonium. Variable induction of TGF-alpha, TGF-beta1, TGF-beta2, and TGF-beta3 gene transcription was evident in the BAMG, with prominent mRNA expression of TGF-alpha and TGF-beta1 6 months after surgery. These cystometric results and detrusor responses to stimulation provide further evidence that graft components do not interfere with host components. Matrix-grafted rat bladders generate, although not increased over time, adequate intravesical pressure responses to produce sustained voiding. Gene expression of different growth factors may be significant in understanding their role in the development and differentiation of the BAMG for partial bladder replacement.

Animals↗

PubMed1998

Functional rat bladder regeneration through xenotransplantation of the bladder acellular matrix graft.

OBJECTIVE: To determine the decreased antigenicity of the bladder acellular matrix graft (BAMG) through xenotransplantation and to assess the in vivo and in vitro functional properties of the rat urinary bladder thus regenerated. MATERIALS AND METHODS: After partial cystectomy (> 50%), BAMGs prepared from hamster, rabbit and dog urinary bladders were grafted to male and female Sprague-Dawley rats; 10 control rats underwent partial cystectomy only. Urinary storage and voiding function were monitored in 15 animals using a specially designed 'micturition cage' and cystometry. After 4 months, organ-bath studies and histological techniques were used to evaluate bladder regeneration in vitro in the grafted animals. RESULTS: Clinically relevant antigenicity was not evident; no animal died from rejection and all bladder wall components regenerated in all BAMG xenografts. However, the degree and quality of regeneration varied. Muscularization, peak pressure, and bladder capacity were higher in the hamster BAMG-grafted animals, whereas in vitro contractility and compliance were best in the dog BAMG-regenerated bladders. All grafted bladders had significantly better capacity and compliance than the autoregenerated bladders after partial cystectomy alone. CONCLUSIONS: The present in vivo and in vitro studies show that BAMG-augmentation cystoplasty can lead to morphological and functional regeneration of the rat bladder, preserving its low-pressure reservoir function. Because BAMG-regenerated bladders show functional innervation that is similar to normal bladders, they can work in coordination with the host bladder components, thus generating adequate intravesical pressure to produce sustained voiding. The decreased antigenicity makes heterologous BAMG transplants feasible without immunosuppression.

Animals↗

PubMed1997

Neurostimulation for bladder evacuation: is sacral root stimulation a substitute for microstimulation?

OBJECTIVE: To determine by anatomical and functional studies whether stimulation of sacral rootlets might permit selective stimulation of autonomic fibres, thus avoiding the detrusor/sphincter dyssynergia characteristic of current techniques of neurostimulation for bladder evacuation. MATERIALS AND METHODS: In 10 male mongrel dogs, the S2 root was isolated and its constituent rootlets followed from their origin in the spinal cord to the point of exit from the dura. The entire root and the individual rootlets were then stimulated, including intra- and extra-dural stimulation and at proximal, mid and distal levels. RESULTS: Neuroanatomical and histological findings showed that rootlets of ventral S2 maintain their identity throughout their intradural course; some carry predominantly autonomic fibres, some predominantly somatic and some a mixture of the two. CONCLUSION: It appears surgically feasible to identify, isolate and sever the predominantly somatic rootlets intradurally, sparing the predominantly autonomic rootlets for inclusion in extradural electrode placement around the entire sacral root, thus eliminating sphincteric interference with detrusor contraction for voiding at low pressure.

Animals↗

PubMed1997

Ecgonine methyl ester, a major cocaine metabolite, causes cerebral vasodilation in neonatal sheep.

Maternal cocaine abuse has been associated with fetal and neonatal neurologic abnormalities, including hemorrhagic cerebral infarctions, but the mechanisms for cocaine's cerebral effects are unknown. We previously showed that acute cocaine injection causes cerebral vasodilation in cats and immature sheep; others have shown that cocaine causes cerebral vasoconstriction in piglets and in pressurized neonatal sheep arteries. Although methodologic and species differences may explain these conflicting results, we tested another possibility; that is, that ecgonine methyl ester (EME), a major cocaine metabolite in sheep, causes cerebral vasodilation and may account, in part, for cocaine's vascular effects. We studied the cerebral effects of a single i.v. injection of EME (2.5 mg/kg) in eight chronically catheterized, unanesthetized neonatal sheep (4 +/- 2 d old). We measured cerebral hemisphere blood flow (CBF) using radiolabeled microspheres, mean arterial pressure, heart rate, and arteriovenous oxygen content, and we calculated cerebral oxygen consumption (CMRo2) and cerebrovascular resistance at baseline and 0.5, 2, 5, and 60 min after EME injection. EME injection had no systemic effects, including no changes in mean arterial pressure, heart rate, or arterial blood gases. Within 0.5 min of injection, EME caused a 21% decrease in cerebrovascular resistance, which remained decreased for 60 min. CBF increased by 20% at 0.5, 2, and 5 min. Blood flow to brain regions other than the cerebral hemispheres paralleled changes in CBF, with cerebellar flow remaining increased at 60 min. There was no change in CMRo2. There was a small, but physiologically insignificant, decrease in arterial oxygen content. We conclude that EME causes cerebral vasodilation in neonatal sheep and may account, in part, for cocaine's cerebral vascular effects.

Animals↗

PubMed1997

Newborn cerebrovascular responses after first trimester moderate maternal ethanol exposure in sheep.

Fetal alcohol syndrome is one of the leading causes of mental retardation in the United States, but the pathogenesis of the associated brain damage is unknown. We tested the hypothesis that neonatal cerebrovascular responses to CO2 and/or hypoxia may be altered by moderate chronic maternal ethanol exposure early in gestation. We studied 26 newborn lambs (1-4 d old). Their mothers had received daily i.v. infusions of either ethanol (1 g/kg; ethanol concentration = 167 +/- 3 mg/dL; mean +/- SEM) or a similar volume of saline for 3 wk during the first trimester. In nine lambs, we studied cerebral responses to CO2 (saline, n = 4; ethanol, n = 5) and in 17 lambs, cerebral responses to hypoxia (saline, n = 7; ethanol, n = 10). Cerebrovascular responses to CO2 were not different between the groups. However, the cerebral vasodilatory response to hypoxemia was significantly attenuated in the ethanol lambs, such that cerebral O2 delivery was not maintained. During severe hypoxia (arterial PO2 = 30 mm Hg), cerebral blood flow increased 106 +/- 23% (mean +/- SEM) above baseline in the saline-treated group, but increased only 32 +/- 15% above baseline in the ethanol-treated group (p < 0.02). Similarly, cerebrovascular resistance in the saline group decreased 52 +/- 6% from baseline, but decreased only 16 +/- 11% in the ethanol group (p < 0.02). We conclude that moderate maternal ethanol infusion early in pregnancy attenuates neonatal hypoxic, but not CO2, cerebrovascular responsivity.

Alcoholism↗

PubMed1996

Neonatology.

Explore the source record for details and available documents.

Anti-Inflammatory Agents↗

PubMed1995

Intraoperative electrostimulation of the cavernous nerve: technique, results and limitations.

PURPOSE: We studied the feasibility of inducing penile erection intraoperatively by stimulation of the cavernous nerves. MATERIALS AND METHODS: In 16 men undergoing retropubic radical prostatectomy and 6 undergoing penile surgery for venous leakage electrostimulation was applied to both sides of the prostatic apex (prostatectomy group) or the hilum of the penis (venous surgery group). RESULTS: Electrostimulation produced visible erection in 8 of the 16 prostatectomy patients and an increase in intracavernous pressure in 5 of the 6 venous surgery patients. CONCLUSIONS: Electrostimulation of the cavernous nerves intraoperatively to produce penile erection is feasible. However, the technique must be further refined to be clinically useful, that is to localize the neurovascular bundle in men undergoing prostatectomy.

Adult↗

PubMed1995

Somatosensory evoked potential and brain water content in post-asphyxic immature piglets.

Depression of somatosensory evoked potentials (SEP) after a single episode of complete asphyxia with near cardiac arrest was evaluated to determine whether persistent SEP depression is related to postresuscitation edema in cortical gray matter or subcortical white matter. Piglets (< 7 d of age) were anesthetized with sodium pentobarbital and fentanyl. Asphyxia was produced by occlusion of the endotracheal tube for 7 min. Arterial O2 saturation fell to 5%. Resuscitation was achieved in < 2 min with ventilation, epinephrine, and chest compressions. Regional brain water content was determined from the difference between wet and dry weight. Two control groups were also analyzed; one immediately after (n = 5) and one 6 h after induction (n = 7) of anesthesia. SEP amplitude became isoelectric during asphyxia and recovered to 50 +/- 13% (n = 7) of baseline 6 h after resuscitation. In the 6-h control group, SEP amplitude remained above baseline. The percent water content (mean +/- SEM) among the three groups (asphyxia versus time control versus brief anesthesia control) was not different in the cortical gray matter (83.0 +/- 0.7% versus 82.4 +/- 0.4% versus 83.2 +/- 0.3%) or subcortical white matter (75.6 +/- 0.8% versus 74.8 +/- 0.9% versus 75.6 +/- 0.5%). In seven other piglets, cerebral blood flow and O2 consumption recovered to baseline by 1 h after asphyxia. Therefore, we found that the sustained depression of SEP amplitude, after 7 min of asphyxia in immature piglets, is not related to brain edema or persistent decreases in global cerebral O2 consumption.

Animals↗

PubMed1995

Cerebral responses to maternal cocaine injection in immature fetal sheep.

Previous studies in near-term sheep have shown that maternal cocaine injection causes acute fetal cerebral vasodilation along with transient hypoxemia and hypertension. Preterm sheep fetuses have lower cerebral O2 consumption (CMRO2) and their cerebrovascular responses to hypoxemia are attenuated compared with near-term fetuses. We therefore tested the hypothesis that fetal cerebrovascular responses to maternal cocaine injection may also differ earlier in gestation. We studied nine immature fetal sheep at 0.65 gestation using the same experimental protocol we used in previous studies in near-term sheep. Fetal studies were done in utero, 2 d after vascular catheter placement. We measured cerebral blood flow (CBF) using microspheres, arterial and sagittal sinus O2 content, and cocaine concentrations. We calculated cerebrovascular resistance (CVR) as mean arterial blood pressure divided by CBF. Measurements were made before and 2, 5, and 15 min after a 2 mg/kg maternal cocaine injection. At 2 min, fetal Cao2 decreased (18 +/- 6%, mean +/- SEM), and there was cerebral vasoconstriction (CVR increased by 22 +/- 5%). At 5 min, CBF increased (19 +/- 9%), but because blood pressure increased also, CVR returned to baseline, and therefore there was no vasodilation compared with baseline. Furthermore, at 5 min there was a 22 +/- 6% decrease in Cao2 and a 21 +/- 6% increase in mean arterial blood pressure. There were no changes in CMRo2 throughout the study, but at 2 min, cerebral O2 delivery decreased. Differences in cerebrovascular responses to maternal cocaine injection earlier in gestation may be due to differences in vascular development and/or to developmental differences in responses to cocaine, cocaine metabolites, and/or to hypoxemia.

Animals↗

PubMed1995

Reinnervation of the rat bladder with a somatic nerve and a striated muscle flap.

PURPOSE: Current techniques of ventral sacral root stimulation to regain voluntary motor control of the decentralized urinary bladder depend upon intact parasympathetic innervation of the detrusor. We investigated techniques that might allow restoration of motor control of the bladder after efferent parasympathetic impairment. MATERIALS AND METHODS: In a chronic rat model, we evaluated whether motor control of a peripherally denervated bladder could be restored by transplantation of autologous excitable tissues and subsequent electrostimulation. Either a somatic nerve or a striated muscle flap was used as the transplant. RESULTS: Four months after the initial surgery, electrostimulation of the somatic nerve implant provoked bladder contractions--a response that was blocked by atropine. Stimulation of the nerve innervating the striated muscle flap also provoked bladder contractions; these were not affected by atropine and were slightly reduced by hexamethonium. CONCLUSION: Reinnervation of the bladder with somatic nerves or striated muscles is possible in principle. Future experiments will clarify the clinical significance of electrostimulation of such implants.

Animals↗