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Biomedical subjects

C E Morris

Publications and source records attributed to C E Morris.

At least 19 recordsLinked to original sources
PubMed2000

The spectrin skeleton of newly-invaginated plasma membrane.

As a cell's shape and volume change. its surface area must re-adjust. How is the plasma membrane's spectrin skeleton implicated? For erythrocytes, cells of fixed surface area, spectrin responses to mechanical disturbances have been studied, but for more typical cells with changeable surface areas, they have not. In rapidly shrinking cells, surface membrane at an adherent substratum invaginates, forming transient vacuole-like dilations (VLDs). We exploited this readily inducible surface area perturbation to pose a simple question: is newly invaginated plasma membrane naked or is it supported by a spectrin skeleton? The spectrin skeleton was examined immunocytochemically in L6 cells (rat skeletal muscle) before and after VLD formation, using fixation in cold methanol and 4112, an antibody against beta-fodrin and beta-spectrin. 4112 was visualized by confocal fluorescence microscopy, while paired phase contrast images independently located the VLDs. To generate VLDs, cells were hypotonically swelled then reshrunk in isotonic medium. Swollen L6 cells maintained their plasma membrane (sarcolemma) spectrin skeleton. Within minutes of subsequent shrinkage, VLDs of 1-2 microm diameter invaginated at the substratum surface of myotubes. Both sarcolemma and VLDs were lined by a relatively uniform spectrin skeleton. Z-series suggested that some of the spectrin skeleton-lined sarcolemma became internalized as vacuoles.

Animals↗
PubMed1999

F-actin at newly invaginated membrane in neurons: implications for surface area regulation.

Neuronal shape and volume changes require accompanying cell surface adjustments. In response to osmotic perturbations, neurons show evidence of surface area regulation; shrinking neurons invaginate membrane at the substratum, pinch off vacuoles, and lower their membrane capacitance. F-actin is implicated in reprocessing newly invaginated membrane because cytochalasin causes the transient shrinking-induced invaginations, vacuole-like dilations (VLDs), to persist indefinitely instead of undergoing recovery. To help determine if cortical F-actin indeed contributes to cell surface area regulation, we test, here, the following hypothesis: invaginating VLD membrane rapidly establishes an association with F-actin and this association contributes to VLD recovery. Cultured molluscan (Lymnaea) neurons, whose large size facilitates three-dimensional imaging, were used. In fixed neurons, fluorescent F-actin stains were imaged. In live neurons, VLD membrane was monitored by brightfield microscopies and actin was monitored via a fluorescent tag. VLD formation (unlike VLD recovery) is cytochalasin insensitive and consistent with this, VLDs formed readily in cytochalasin-treated neurons but showed no association with F-actin. Normally, however (i.e., no cytochalasin), VLDs were foci for rapid reorganization of F-actin. At earliest detection (1-2 min), nascent VLDs were entirely coated with F-actin and by 5 min, VLD mouths (i.e. , at the substratum) had become annuli of F-actin-rich motile leading edge. Time lapse images from live neurons showed these rings to be motile filopodia and lamellipodia. The retrieval of VLD membrane (vacuolization) occurred via actin-associated constriction of VLD mouths. The interplay of surface membrane and cortical cytoskeleton in osmotically perturbed neurons suggests that cell surface area and volume adjustments are coordinated in part via mechanosensitive F-actin dynamics.

Actins↗
PubMed1999

Membrane stretch affects gating modes of a skeletal muscle sodium channel.

The alpha subunit of the human skeletal muscle Na(+) channel recorded from cell-attached patches yielded, as expected for Xenopus oocytes, two current components that were stable for tens of minutes during 0.2 Hz stimulation. Within seconds of applying sustained stretch, however, the slower component began decreasing and, depending on stretch intensity, disappeared in 1-3 min. Simultaneously, the faster current increased. The resulting fast current kinetics and voltage sensitivity were indistinguishable from the fast components 1) left after 10 Hz depolarizations, and 2) that dominated when alpha subunit was co-expressed with human beta1 subunit. Although high frequency depolarization-induced loss of slow current was reversible, the stretch-induced slow-to-fast conversion was irreversible. The conclusion that stretch converted a single population of alpha subunits from an abnormal slow to a bona fide fast gating mode was confirmed by using gigaohm seals formed without suction, in which fast gating was originally absent. For brain Na(+) channels, co-expressing G proteins with the channel alpha subunit yields slow gating. Because both stretch and beta1 subunits induced the fast gating mode, perhaps they do so by minimizing alpha subunit interactions with G proteins or with other regulatory molecules available in oocyte membrane. Because of the possible involvement of oocyte molecules, it remains to be determined whether the Na(+) channel alpha subunit was directly or secondarily susceptible to bilayer tension.

Amino Acid Sequence↗
PubMed1999

Chiropractic rehabilitation of a patient with S1 radiculopathy associated with a large lumbar disk herniation.

OBJECTIVE: To describe the nonsurgical treatment of acute S1 radiculopathy from a large (12 x 12 x 13 mm) L5-S1 disk herniation. CLINICAL FEATURES: A 31-year-old man presented with severe lower back pain and pain, paresthesia, and plantar flexion weakness of the left leg. His symptoms began 5 days before the initial visit and progressed despite nonsteroidal anti-inflammatory drugs and analgesic medication. An absent left Achilles reflex, left S1 dermatome hypesthesia, and left gastrocnemius/soleus weakness was noted. Magnetic resonance imaging demonstrated a large L5-S1 disk herniation. INTERVENTION AND OUTCOME: Initial treatment of this patient included McKenzie protocol press-ups to reduce and centralize symptoms, nonloading exercise for cardiovascular fitness, and lower leg isotonic exercises to prevent atrophy. Counseling was provided to reduce abnormal illness behavior risk. Later, flexion distraction and side-posture manipulation were provided to improve joint function. Sensory motor training, trunk stabilization exercises, and trigger point therapy were also used. He returned to modified work 27 days after symptom onset. A follow-up, comparative magnetic resonance imaging (MRI) study was unchanged. He was discharged as symptomatic (zero rating on both the Oswestry and numerical pain scales) after 50 days and 20 visits, although the left S1 reflex remained absent. Reassessment 169 days later revealed neither significant symptoms nor lifestyle restrictions. CONCLUSION: This case demonstrates the potential benefit of a chiropractic rehabilitation strategy by use of multimodal therapy for lumbar radiculopathy associated with disk herniation.

Adult↗
PubMed1999

Activation of mechanosensitive currents in traumatized membrane.

Mechanosensitive (MS) channels, ones whose open probability varies with membrane tension in patch recordings, are diverse and ubiquitous, yet many are remarkably insensitive to mechanical stimuli in situ. Failure to elicit mechanocurrents from cells with abundant MS channels suggests that, in situ, the channels are protected from mechanical stimuli. To establish what conditions affect MS channel gating, we monitored Lymnaea neuron stretch-activated K (SAK) channels in cell-attached patches after diverse treatments. Mechanosensitivity was gauged by rapidity of onset and extent of channel activation during a step pressure applied to a "naive" patch. The following treatments enhanced mechanosensitivity: actin depolymerization (cytochalasin B), N-ethylmaleimide, an inhibitor of ATPases including myosin, elevated Ca (using A-23187), and osmotic swelling (acutely and after 24 h). Osmotic shrinking decreased mechanosensitivity. A unifying interpretation is that traumatized cortical cytoskeleton cannot prevent transmission of mechanical stimuli to plasma membrane channels. Mechanoprotection and capricious mechanosensitivity are impediments to cloning efforts with MS channels. We demonstrate a potpourri of endogenous MS currents from L-M(TK-) fibroblasts; others had reported these cells to be MS current null and hence to be suitable for expressing putative MS channels.

Animals↗
PubMed1999

Gender and effect of impact acceleration on neck motion.

BACKGROUND: With the opening of the fighter cockpit to women, it became imperative to expand the current database of responses of females to both sustained and impact acceleration environments. With less upper-body strength (lean body mass) than men, it was hypothesized that women would not brace their heads as effectively against the loads occurring during high G-loading in flight and during impact and escape. This scenario creates increased potential for injury, exacerbated by the changing center of gravity and weight of helmets due to technological advances (e.g., night vision, head-up displays, etc.). METHODS: The main objective of this experimental effort was measuring the ability of subjects of both sexes to brace against an impact acceleration of -6.5 Gx or +4.0 Gy. An attempt was made to identify a correlation between such ability, static strength measurements, anthropometric measurements, or any combination thereof. RESULTS: No correlation was found between any of the static strength or anthropomorphic parameters and the amplitude of head motion. The isometric strength measurements correlated well with the size, weight, and neck circumference of the subjects, but none of these proved useful in predicting head displacement. However, there was a strong relationship between neck force exerted just before impact and head motion in the -Gx study, and somewhat less correlation for the +Gy impacts. CONCLUSION: It is useful to estimate resistance to impact by measuring neck strength, but only under conditions where the subject is highly motivated.

Acceleration↗
PubMed1998

Neuronal plasma membrane dynamics evoked by osmomechanical perturbations.

When neurons swell and shrink they extensively reorganize their plasma membrane. A striking aspect of these membrane dynamics is the transient appearance of vacuole-like dilations (VLDs) which, counterintuitively, expand as the neurons shrink. Here, confocal microscopy of cultured molluscan (Lymnaea) neurons was used in conjunction with aqueous phase and membrane dyes to examine changing VLD membrane topology as VLDs form, reverse or recover. We show that VLDs start as discrete invaginations at the adherent surface, so VLD and plasma membranes are initially contiguous. Over the next few minutes VLDs expand and penetrate the cytoplasm. At the substratum, the mouths of VLDs develop into irregular annuli of motile adherent processes whereas deeper in the cytoplasm, VLD membrane profiles are smooth. Subsequently VLDs spontaneously shrink; as this recovery proceeds, constriction of the motile VLD mouth leads to the internalization of plasma membrane. Washout experiments with aqueous phase dyes demonstrated that VLD constriction yields bona fide vacuoles, i.e., membrane-bound compartments isolated from the external medium. VLDs can also be experimentally eliminated by returning cells to swelling conditions; this reversal process drives membrane back to the surface. VLD formation and reinternalization of VLD membrane can be seen as aspects of plasma membrane surface area regulation. We postulate that area adjustments, driven by regional membrane tension differences, become noticeable when excessive perturbations overload normal membrane reprocessing steps. Both the changes in VLD membrane topology, and previously established capacitance changes accompanying cell shrinking and swelling, argue that osmomechanically perturbed neurons regulate their surface area as their volume changes.

Animals↗
PubMed1998

Membrane tension in swelling and shrinking molluscan neurons.

When neurons undergo dramatic shape and volume changes, how is surface area adjusted appropriately? The membrane tension hypothesis-namely that high tensions favor recruitment of membrane to the surface whereas low tensions favor retrieval-provides a simple conceptual framework for surface area homeostasis. With membrane tension and area in a feedback loop, tension extremes may be averted even during excessive mechanical load variations. We tested this by measuring apparent membrane tension of swelling and shrinking Lymnaea neurons. With hypotonic medium (50%), tension that was calculated from membrane tether forces increased from 0.04 to as much as 0.4 mN/m, although at steady state, swollen-cell tension (0. 12 mN/m) exceeded controls only threefold. On reshrinking in isotonic medium, tension reduced to 0.02 mN/m, and at the substratum, membrane invaginated, creating transient vacuole-like dilations. Swelling increased membrane tension with or without BAPTA chelating cytoplasmic Ca2+, but with BAPTA, unmeasurably large (although not lytic) tension surges occurred in approximately two-thirds of neurons. Furthermore, in unarborized neurons voltage-clamped by perforated-patch in 50% medium, membrane capacitance increased 8%, which is indicative of increasing membrane area. The relatively damped swelling-tension responses of Lymnaea neurons (no BAPTA) were consistent with feedback regulation. BAPTA did not alter resting membrane tension, but the large surges during swelling of BAPTA-loaded neurons demonstrated that 50% medium was inherently treacherous and that tension regulation was impaired by subnormal cytoplasmic [Ca2+]. However, neurons did survive tension surges in the absence of Ca2+ signaling. The mechanism to avoid high-tension rupture may be the direct tension-driven recruitment of membrane stores.

Animals↗
PubMed1998

Neuronal swelling and surface area regulation: elevated intracellular calcium is not a requirement.

Neurons are mechanically robust. During prolonged swelling, molluscan neurons can triple their apparent membrane area. They gain surface area and capacitance independent of extracellular Ca concentration ([Ca]e), but it is unknown if an increase in intracellular Ca concentration ([Ca]i) is necessary. If Ca for stimulating exocytosis is unnecessary, it is possible that swelling-induced membrane tension changes directly trigger surface area readjustments. If, however, Ca-mediated but not tension-mediated membrane recruitment is responsible for surface area increases, swelling neurons should sustain elevated levels of [Ca]i. The purpose of this investigation is to determine if the [Ca]i in swelling neurons attains levels high enough to promote exocytosis and if any such increase is required. Lymnaea neurons were loaded with the Ca concentration indicator fura 2. Calibration was performed in situ using 4-bromo-A-23187 and Ca-ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA), with free Ca concentration ranging from 0 to 5 microM. Swelling perturbations (medium osmolarity reduced to 25% for 5 min) were done at either a standard [Ca]e or very low [Ca]e level (0.9 mM or 0.13 microM, respectively). In neither case did the [Ca]i increase to levels that drive exocytosis. We also monitored osmomechanically driven membrane dynamics [swelling, then formation and reversal of vacuole-like dilations (VLDs)] with the [Ca]i clamped below 40 nM via 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA). [Ca]i did not change with swelling, and VLD behavior was unaffected, consistent with tension-driven, [Ca]i-independent surface area adjustments. In addition, neurons with [Ca]i clamped at 0.1 microM via an ionophore could produce VLDs. We conclude that, under mechanical stress, neuronal membranes are compliant by virtue of surface area regulatory adjustments that operate independent of [Ca]i. The findings support the hypothesis that plasma membrane area is regulated in part by membrane tension.

Animals↗
PubMed1998

Transepithelial transport of nicotine and vinblastine in isolated malpighian tubules of the tobacco hornworm (Manduca sexta) suggests a P-glycoprotein-like mechanism.

We have examined the accumulative transport properties of the Malpighian (excretory) tubules of the tobacco hornworm Manduca sexta to test the hypothesis that a P-glycoprotein-like multidrug transporter is active and is responsible for the excretion of dietary nicotine in this tissue. Isolated tubules were cannulated and exposed to radiolabelled forms of either nicotine (5 min exposure) or the P-glycoprotein substrate vinblastine (60 min exposure) in the bathing (basal surface) fluid. The luminal (apical) contents were then flushed, and lumen-to-bath ratios were measured. Although these ratios provide conservative estimates of the physiological ability of Malpighian tubules to move compounds from blood to lumen, tubules concentrated nicotine 10-fold from an initial bath concentration of 0.5 mmol l-1 and vinblastine threefold (from an initial concentration of 1 micromol l-1). Vectorial transport of vinblastine and nicotine was eliminated by 25 micromol l-1 verapamil (a P-glycoprotein inhibitor) and was not dependent on the presence of a transepithelial electrical potential. Nicotine transport was inhibited by atropine (3 mmol l-1), while nicotine (> or = 50 micromol l-1) significantly reduced vinblastine transport. Verapamil was effective at reducing vinblastine transport when applied to the basal side alone, but not when applied to the apical side alone. Taken together, these results are consistent with the idea that the active excretion of nicotine and other alkaloids by the tobacco hornworm is mediated by a P-glycoprotein-like mechanism.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1997

Initial and steady-state effects of diphenhydramine and loratadine on sedation, cognition, mood, and psychomotor performance.

BACKGROUND: The classic, first-generation histamine1-receptor antagonists used to treat allergic disorders frequently cause sedation. In contrast, sedation is reduced or absent after administration of recommended doses of second-generation histamine1-receptor antagonists. We measured the initial and steady-state effects of diphenhydramine, a first-generation antihistamine, and loratadine, a second-generation antihistamine, by means of a comprehensive battery of psychometric tests that mirror real-world tasks. METHODS: Healthy volunteers (N = 98) were randomly assigned in a double-blind fashion to receive loratadine (n = 33), diphenhydramine (n = 32), or placebo (n = 33). A computerized test battery was administered at baseline, on day 1 after administration of the initial dose, and on days 3 and 5. RESULTS: After the initial dose, subjects taking diphenhydramine demonstrated poorer cognitive performance than subjects taking loratadine or placebo on tasks of divided attention, working memory, speed, and vigilance. Subjects taking diphenhydramine also reported greater fatigue and sleepiness and lower levels of motivation, and rated the quality of their performance as lower than subjects taking loratadine or placebo. On day 3, subjects taking diphenhydramine continued to show more fatigue and lower motivation, and rated the quality of their test performance as poorer than subjects taking loratadine or placebo. There were no differences between loratadine and placebo after the initial dose or steady-state (day 5) dosing for any measure of cognitive or psychomotor test performance, mood, or sedation. CONCLUSIONS: Patients taking diphenhydramine may be at risk of lapses and significant errors that may lead to potential hazards and decreased work productivity.

Adult↗
PubMed1997

Human subject research at Armstrong Laboratory, 1973-93: medical and musculoskeletal disqualifications.

The reasons for disqualification of human subjects from 1973-93 at Armstrong Laboratory, formerly the Harry G. Armstrong Aeromedical Research Laboratory (AAMRL), are presented for both sustained and impact acceleration panels. Evaluations for both medical and spinal anomalies were accomplished. The rationale for each disqualification is discussed, demonstrating the variability in each panel physician's clinical judgment in the context of personal bias, the ethical framework surrounding the use of human volunteers, and the existing research milieu.

Acceleration↗
PubMed1997

Comparison of acceleration subjects to other populations: spinal anomaly distribution.

Two Armstrong Laboratory (AL) human volunteer subject panels (sustained and impact acceleration) at Wright Patterson AFB, OH, were compared to each other and to other samples of different populations in terms of spinal anomalies. These sample populations were obtained from the scientific literature: French, Norwegian, Netherlands, and U.S. pilots; U.S. Air Force (AF) and Navy subjects, and from representative "normal" civilian populations, and then compared using the proportion parameters for various spinal anomalies. There were only a few common parameters between the two panels and between each panel compared with the foreign military, human subjects, and "normal" population. However, there were two to six times as many similar spinal anomaly incidence rates between the AL panels and the U.S. pilot sample. It was reassuring that the AL subject panels used in AF acceleration research have more in common with AF pilots than other populations in regards to spinal anomalies, even though the pilot sample may not be representative of the true pilot population. Recommendations are to establish a common reference point in nomenclature and description of spinal anomalies (modeled after the French) and to start collecting spinal radiographs on all U.S. pilots. These radiographs would not be for screening but for establishing a database following the occupational pathology of flying. This data would also facilitate comparisons with research acceleration panels, as well as with foreign air forces. Informed decisions can then be made regarding screening criteria for the future as aircraft and ejection seat performance envelopes continue to expand.

Acceleration↗
PubMed1997

Are human subject volunteers still players in aeromedical research as we enter the 21st century?

The U.S. Air Force has enjoyed the luxury of having dedicated human volunteer subjects for sustained and impact acceleration research for over 50 yr. However, with today's world economy and budgetary cutbacks, this may no longer be a viable option. The onslaught of advanced medical technology, combined with an increasing performance envelope for aircraft and their ejection systems, have created an environment where the validity of research data and the ethics of human-use research are being challenged. Now is an opportune time to reevaluate the way human-use aeromedical research is conducted. The validity of using nonpilots in lieu of pilots in aeromedical research is discussed in light of the following: a) the increased emphasis on performance metrics within sustained acceleration; b) the matching of human subjects (nonpilots) to pilots in the appropriate attributes to ensure validity of data; c) degree of medical screening required given the ethics of human-use research and concerns of pilots; and d) the challenge of evaluating the "value added" of new technology for medical screening. It is concluded that volunteer panels should be maintained with nonpilots matched with pilots physically and psychologically such that operational performance characteristics are similar. Medical screening should be similar so that research data from subjects can be applied to the target population (pilots). Longitudinal data collection (e.g., spinal X-rays) on pilots would also be of great value as a basis for studying the occupational hazards of flying.

Acceleration↗
PubMed1997

Human subject screening: a dynamic process.

INTRODUCTION: The history of disqualified (DQ) subjects from 1973-1993 at Armstrong Laboratory, Wright Patterson AFB, is presented for both sustained and impact acceleration panels. METHODS: Candidate and subject medical records were reviewed for screening results, recommendation for panel duty, and any follow-up medical findings. The generation and interpretation of the medical screening criteria and DQ rates are discussed. MEDICAL SCREENING CRITERIA: The mechanisms for change, those factors influencing change, and the interpretation of the screening criteria for Armstrong Laboratory's acceleration panels determine the panel's composition, which is reflected in the DQ rates. RESULTS: The centrifuge had a 5% (7/132) disqualification (DQ) rate from 1973-93 with 29% (2/7) due to musculoskeletal and 71% (5/7) for medical reasons. All were DQ during 1973-88. The impact panel had a DQ rate of 18% (36/195) with 71% (24/34) DQ due to musculoskeletal and 29% (10/34) for medical reasons. Only 28% (10/36) were DQ during 1973-88, while during 1989-93, 72% (26/36) were DQ. CONCLUSIONS: The differences in DQ rates between the centrifuge and impact facility were due to the variability or conservatism of individual physicians, interpretation of the medical screening criteria, and the type of research being done. These factors effect the composition of the human subject panels. This determines to which target population the research data can be applied. If the subjects do not represent pilots due to inappropriate screening, then there is no benefit from the research and, therefore, there can be no risk incurred by the subjects.

Acceleration↗
PubMed1996

Coiled mechanoreceptors in Aplysia revealed by sensorin immunofluorescence and confocal microscopy.

Identified mechanosensory neurons of Aplysia are established model neurons for studies on learning and memory, and for examining responses to axonal injury. Although many characteristics of these sensory neurons have received intensive study, the nature of the peripheral mechanoreceptive endings remains unknown. Identification of a peptide, sensorin, specific in Aplysia for mechanosensory neurons, led to the development of an antibody which proved useful in studying the peripheral morphology of these neurons. Immunostaining for sensorin in tail body wall revealed that sensorin is present in peripheral arborizations. Examination of sensorin-positive fibers in the periphery revealed that they terminate as coiled structures in the muscle layer of the body wall. These coiled structures (approximately 0.5 microns diameter processes, 2-3 microns across the coil, approximately 60 microns long) run parallel to muscle fibers and have a pitch of about one turn per 4 microns. Sensorin immunostaining was particularly intense in varicosities, both along peripheral fibers and along the coiled structure. The localization of sensorin suggests that it may be released peripherally where it could have various paracrine and/or autocrine neuromodulatory actions.

Animals↗
PubMed1995

Responses of neurons to extreme osmomechanical stress.

Neurons are often regarded as fragile cells, easily destroyed by mechanical and osmotic insult. The results presented here demonstrate that this perception needs revision. Using extreme osmotic swelling, we show that molluscan neurons are astonishingly robust. In distilled water, a heterogeneous population of Lymnaea stagnalis CNS neurons swelled to several times their initial volume, yet had a ST50 (survival time for 50% of cells) > 60 min. Cells that were initially bigger survived longer. On return to normal medium, survivors were able, over the next 24 hr, to rearborize. Reversible membrane capacitance changes corresponding to about 0.7 muF/cm2 of apparent surface area accompanied neuronal swelling and shrinking in hypo- and hyperosmotic solutions; reversible changes in cell surface area evidently contributed to the neurons' ability to accommodate hydrostatic pressures then recover. The reversible membrane area/capacitance changes were not dependent on extracellular Ca2+. Neurons were monitored for potassium currents during direct mechanical inflation and during osmotically driven inflation. The latter but not the former stimulus routinely elicited small potassium currents, suggesting that tension increases activate the currents only if additional disruption of the cortex has occurred. Under stress in distilled water, a third of the neurons displayed a quite unexpected behavior: prolonged writhing of peripheral regions of the soma. This suggested that a plasma membrane-linked contractile machinery (presumably actomyosin) might contribute to the neurons' mechano-osmotic robustness by restricting water influx. Consistent with this possibility, 1 mM N-ethyl-maleimide, which inhibits myosin ATPase, decreased the ST50 to 18 min, rendered the survival time independent of initial size, and abolished writhing activity. For neurons, active mechanical resistance of the submembranous cortex, along with the mechanical compliance supplied by insertion or eversion of membrane stores may account for the ability to withstand diverse mechanical stresses. Mechanical robustness such as that displayed here could be an asset during neuronal outgrowth or regeneration.

Animals↗