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PubMed1989

Structural changes in airways of rats exposed to nitrogen dioxide intermittently for seven days. Comparison between major bronchi and terminal bronchioles.

Structural changes caused by exposure to NO2 were compared between the largest intrapulmonary bronchi (major bronchi) and the terminal bronchioles. Rats were exposed to 50 ppm NO2 for 5 h a day for 7 consecutive days, and microscopic findings were assessed subjectively and quantitatively. Destruction of airway epithelium was present on Day 1, and the reparative phase was observed between Days 3 and 7. Light microscopy showed that on Day 1, loss of cilia and disintegration of epithelium occurred, and that the latter was worse in major bronchi than in terminal bronchioles; apical projections of Clara cells in terminal bronchioles were lost almost totally. Recovery of epithelium began by Day 3 and cilia by Day 5, and ciliogenesis progressed less promptly in terminal bronchioles. Clara cells did not return to normal during the experiment. Furthermore, a decrease in the airway diameter occurred in peripheral airways along with an increase in mural thickness in terminal bronchioles. Mural inflammation was also seen more conspicuously in terminal bronchioles. Electron microscopy revealed that epithelial cells lost secretory granules on Day 1 and began to repair them by Day 5 in major bronchi and by Day 7 in terminal bronchioles. It is likely that epithelium in terminal bronchioles is not particularly sensitive to NO2 compared with that in major bronchi, but that recovery occurs more promptly in major bronchi than in terminal bronchioles. Mechanisms underlying bronchoconstriction occurring preferentially in peripheral airways are also discussed.

Animals↗

PubMed2003

Interrelationships between structural parameters of cancellous bone reveal accelerated structural change at low bone volume.

UNLABELLED: This study shows that change to cancellous bone structure is bone volume-dependent in a nonlinear manner. At low bone volume (< 15%), trabecular thickness and trabecular separation change at a much greater rate than at higher bone volume. This suggests that the structural integrity of the cancellous bone may become rapidly compromised when bone volume falls below a critical value. INTRODUCTION: While bone mass is the major determinant of bone strength, this mass-based paradigm does not fully account for the contribution of the bone microstructure to mechanical efficiency. Geometric models of cancellous bone structure have been formulated based on stylized representations of the trabecular elements, where the relationships between bone volume and bone surface of cancellous bone are complex and reflect the modulating effect on the cancellous bone structure of bone remodeling at the trabecular surfaces. Using the plate model of cancellous bone structure, the interrelationships between parameters of cancellous bone structure have been studied. MATERIALS AND METHODS: Two hundred eighty histological sections of human cancellous bone from eight skeletal sites were analyzed. The structural parameters of cancellous bone (BV/TV, BS/TV, BS/BV, Tb.Th, Tb.Sp, Tb.N, and TBPf) were obtained. RESULTS AND CONCLUSIONS: This study shows that change to cancellous bone structure is bone volume-dependent in a nonlinear manner. At low bone volume (< 15%), structural parameters of cancellous bone, such as trabecular thickness and trabecular separation, change at a much greater rate than at higher bone volume. This suggests that the structural integrity of the cancellous bone may become rapidly compromised when bone volume falls below a critical value. These data describe the complex relationships between bone mass and structure in cancellous bone that are often overlooked in the mass-based paradigm of bone strength. Histomorphometric descriptors of cancellous bone structure highlight the potential for accelerated deterioration of the structure with low bone volume, which leads to increased risk of fracture. From a clinical viewpoint, estimation of an individual's fracture risk is constrained to noninvasive techniques, which only provide bone mineral density or bone mineral content. Therefore, there is a need to better correlate measurement of bone mass with measurements of structural parameters.

Bone Density↗

PubMed1984

[Structural changes and hemodynamic relations in the microcirculatory bed of the mesentery of the white rat during the period of sexual maturation].

Structural changes and hemodynamic relations have been studied in the microcirculatory bed of the white rat small intestine mesentery during sex maturation (from the 3d up to the 10th week of the postnatal development). All calculations are performed regarding the mesenteric segment limited with two intestinal arteries, which is considered as an elementary microvascular module. Complication of the microcirculatory bed construction takes place at the expense of increasing number (nearly five-fold) of microvessels in the segment and increase of the capillary network density. The hemodynamic factor plays a certain role for stimulating the process of the capillary growth. The definitive structure of the mesenteric microcirculatory bed is completed by the 7th week. The main rearrangement of the microcirculatory system during the developmental process from a simple arterio-venular loop up to a complex microcirculatory bed with a branching capillary network is performed within the limits of the mesenteric segment.

Animals↗

PubMed1999

The ligand-induced structural changes of human L-Arginine:Glycine amidinotransferase. A mutational and crystallographic study.

Human L-arginine:glycine amidinotransferase (AT) shows large structural changes of the 300-flap and of helix H9 upon binding of L-arginine and L-ornithine, described as a closed and an open conformation (Humm, A., Fritsche, E., Steinbacher, S., and Huber, R. (1997) EMBO J. 16, 3373-3385). To elucidate the structural basis of these induced-fit movements, the x-ray structures of AT in complex with the amidino acceptor glycine and its analogs gamma-aminobutyric acid and delta-aminovaleric acid, as well as in complex with the amidino donor analogs L-alanine, L-alpha-aminobutyric acid, and L-norvaline, have been solved at 2.6-, 2.5-, 2.37-, 2.3-, 2.5-, and 2.4-A resolutions, respectively. The latter three compounds were found to stabilize the open conformer. The glycine analogs bind in a distinct manner and do not induce the transition to the open state. The complex with glycine revealed a third binding mode, reflecting the rather broad substrate specificity of AT. These findings identified a role for the alpha-amino group of the ligand in stabilizing the open conformer. The kinetic, structural, and thermodynamic properties of the mutants ATDeltaM302 and ATDelta11 (lacks 11 residues of H9) confirmed the key role of Asn300 and suggest that in mammalian amidinotransferases, the role of helix H9 is in accelerating amidino transfer by an induced-fit mechanism. Helix H9 does not add to the stability of the protein.

Amidinotransferases↗

PubMed1996

Arterial stiffening: opposing effects of age- and hypertension-associated structural changes.

This article reviews the effects of aging and hypertension on geometrical (lumen and arterial wall thickness) and functional (distensibility) properties of large and medium-sized arteries in humans. Several clinical and animal studies show that arterial wall hypertrophy does not increase the elastic modulus of the arterial wall material during sustained essential hypertension. The structural changes associated with either hypertension or aging have opposing effects on arterial distensibility, under similar transmural conditions: the former increasing it, the latter decreasing it. Thus, hypertension cannot be assimilated to aging. The structural and functional changes of the arterial wall material that are associated with the hypertension-induced hypertrophy could be a means by which medium-sized arteries maintain their distensibility characteristics despite increased distending pressure, and large arteries compensate for the age-induced decrease in arterial compliance.

Aging↗

PubMed2003

Evidence for structural changes in carboxyl-terminal peptides of transducin alpha-subunit upon binding a soluble mimic of light-activated rhodopsin.

Although a high-resolution crystal structure for the ground state of rhodopsin is now available, portions of the cytoplasmic surface are not well resolved, and the structural basis for the interaction of the cytoplasmic loops with the retinal G-protein transducin (G(t)) is still unknown. Previous efforts aimed at the design, construction, and functional characterization of soluble mimics for the light-activated state of rhodopsin have shown that grafting defined segments from the cytoplasmic region of bovine opsin onto a surface loop in a mutant form of thioredoxin (HPTRX) is sufficient to confer partial G(t) activating potential [Abdulaev et al. (2000) J. Biol. Chem. 275, 39354-39363]. To assess whether these designed mimics could provide a structural insight into the interaction between light-activated rhodopsin and G(t), the ability of an HPTRX fusion protein comprised of the second (CD) and third (EF) cytoplasmic loops (HPTRX/CDEF) to bind G(t) alpha-subunit (G(t)(alpha)) peptides was examined using nuclear magnetic resonance (NMR) spectroscopy. Transfer NOESY (TrNOESY) experiments show that an 11 amino acid peptide corresponding to the carboxyl terminus of G(t)(alpha) (GtP), as well as a "high-affinity" peptide analogue, HAP1, binds to HPTRX/CDEF in the fast-exchange regime and undergoes similar, subtle structural changes at the extreme carboxyl terminus. Observed TrNOEs suggest that both peptides when bound to HPTRX/CDEF adopt a reverse turn that is consistent with the C-cap structure that has been previously reported for the interaction of GtP with the light-activated signaling state, metarhodopsin II (MII). In contrast, TrNOESY spectra provide no evidence for structuring of the amino terminus of either GtP or HAP1 when bound to HPTRX/CDEF, nor do the spectra show any measurable changes in the CD and EF loop resonances of HPTRX/CDEF, which are conformationally dynamic and significantly exchange broadened. Taken together, the NMR observations indicate that HPTRX/CDEF, previously identified as a functional mimic of MII, is also an approximate structural mimic for this light-activated state of rhodopsin.

Animals↗

PubMed2002

Relationship between microalbuminuria and cardiac structural changes in mild hypertensive patients.

The aim of this study was to determine the relationship between urinary albumin excretion (UAE), cardiac structural changes upon echocardiography and 24-h ambulatory blood pressure (ABPM) levels. Twenty mild hypertensive patients (mean age 56.8 +/- 9.6 years) were evaluated. After 2 weeks of a washout period of all antihypertensive drugs, all patients underwent an echocardiographic evaluation, a 24-h ABPM and an overnight urine collection. Systolic and diastolic blood pressure during 24-h ABPM was 145 +/- 14/91 +/- 10 mmHg (daytime) and 130 +/- 14/76 +/- 8 mmHg (nighttime), respectively. Seven (35%) patients presented UAE > or = 15 microg/min, and for the whole group, the geometric mean value for UAE was 10.2 x// 3.86 microg/min. Cardiac measurements showed mean values of interventricular septum thickness (IVS) of 11 +/- 2.3 mm, left ventricular posterior wall thickness (PWT) of 10 +/- 2.0 mm, left ventricular mass (LVM) of 165 +/- 52 g, and left ventricular mass index (LVMI) of 99 +/- 31 g/m2. A forward stepwise regression model indicated that blood pressure levels did not influence UAE. Significant correlations were observed between UAE and cardiac structural parameters such as IVS (r = 0.71, P<0.001), PWT (r = 0.64, P<0.005), LVM (r = 0.65, P<0.005) and LVMI (r = 0.57, P<0.01). Compared with normoalbuminuric patients, those who had microalbuminuria presented higher values of all cardiac parameters measured. The predictive positive and negative values of UAE > or = 15 microg/min for the presence of geometric cardiac abnormalities were 75 and 91.6%. These data indicate that microalbuminuria in essential hypertension represents an early marker of cardiac structural damage.

Adult↗

PubMed1987

Thyroid and pituitary secretory disorders in streptozotocin-diabetic rats are associated with severe structural changes of these glands.

Streptozotocin diabetes in rats is associated with reduced function of the hypothalamo-pituitary-thyroid axis. The structure and hormone secretion of the thyroid and pituitary glands were studied in adult male rats 1 month after streptozotocin injection. The thyroid of diabetic rats was characterized by decreased follicle area and epithelial thickness. By electron microscopy, thyroid epithelial cells were characterized by flattened and almost empty rough endoplasmic reticulum cisternae, scanty exocytotic apical and endocytotic vesicles as well as degenerate mitochondria and rough endoplasmic reticulum. By immunohistochemistry, intracolloidal thyroglobulin and T3 as well as intraepithelial thyroglobulin were reduced. Electron microscopic and immunohistochemical analysis of pituitary glands showed that in diabetic rats thyrotrophs were mostly of type II, and the number of thyrotrophs (type I + type II) was greater than in controls. By radioimmunoassay (RIA), plasma T3, T4, and TSH levels were markedly reduced, and the TSH response to TRH was deficient in diabetic animals. The pituitary TSH concentration was increased, as expected from the morphological data. This study demonstrates severe structural changes in the thyroid and pituitary glands of diabetic rats which are accompanied by marked alterations of their secretory activity.

Animals↗

PubMed1991

Structural changes in the airways of sensitized brown Norway rats after antigen challenge.

The purpose of this study was to quantitate the structural changes in the airways of sensitized rats after repeated challenge with aerosolized antigen and to examine the relationship between these changes and alterations in responsiveness to methacholine (MCh). We studied 28 Brown Norway rats that were actively sensitized to ovalbumin (OA). Responsiveness to aerosolized MCh was quantitated as the concentration of MCh required to double pulmonary resistance (EC200 RL). The EC200 RL was determined before and 1 and 5 days after three inhalational challenges with OA (n = 17) or saline (n = 11) at 5-day intervals (on Days 14, 19, and 24 after sensitization). Responsiveness to MCh increased after OA; EC200 RL fell from 1.71 to 0.71 mg/ml at 1 day (p less than 0.01) and 0.87 mg/ml at 5 days (p less than 0.02) after OA but did not change after saline challenge. Formalin-fixed lungs from a sample of OA-challenged (n = 12) and saline-challenged (n = 6) animals were paraffin embedded, and 5-microns sections were stained with hematoxylin-phloxin-saffron. Cross-sectional areas of the airway wall and smooth muscle (ASM) were determined for all intrapulmonary membranous airways. There was an approximately twofold increase in the quantity of airway smooth muscle in airways of OA-challenged animals compared with saline-challenged control animals. Airway wall area did not change significantly. There was a correlation (r = 0.618, p less than 0.05) between the quantity of ASM in large airways (basement membrane length 2.00 to 2.99 mm) and change in responsiveness to MCh.

Animals↗

PubMed2000

Structural changes of neurons in hippocampus from infantile rats exposed to hyperbaric oxygen.

OBJECTIVE: To investigate if hyperbaric oxygen ( HBO) may induce structural changes of neurons in hippocampus from infantile rats and if the changes are reversible. METHODS: All 27 healthy SD infantile rats were exposed to HBO (0.25 MPa) or hyperbaric air (HBA) for 1 to 3 courses (10 days as 1 course). The hippocampus was taken at the end of each course to observe its morphology b y light microscope and electron microscope. RESULTS: HBO exposure induced capillary dilation, nuclear membr ane winding or blurring and some mitochondria swelling with its crista blurring i n neurons. The changes occurred after 1 course exposure and became significant w ith time. Most of the changes recovered 20 days after stopping exposure. No chan ge was found after HBA exposure. CONCLUSIONS: Long-term HBO exposure can cause capillary dilati on and ultrastructural injury of neurons in hippocampus from infantile rats. The damage is not serious, but reversible.

Journal Article↗

PubMed1977

Gap junctions. Structural changes after uncoupling procedures.

The freeze-fracture appearance of rat stomach and liver gap junctions changes after uncoupling procedures such as inhibition of the metabolism of perfusion with hypertonic sucrose. In control stomach, either fixed immediately or kept for 1 h in a well-oxygenated Tyrode's solution at 37 degrees C, most gap junctions between mucous cells contain particles irregularly packed at an average center-to-center spacing of 10.3-10.5 nm. After 1-h treatment with 2,4-dinitrophenol (DNP), at the same temperature and oxygenation, most particles aggregate hexagonally at an average spacing of approximately 8.5 nm. Similar changes are seen in hypoxic specimens. In control liver, fixed by perfusion, most junctional particles are irregularly packed at an average center-to-center spacing of approximately 10 mm. Small areas of fairly regular hexagonal packing are occasionally seen, where the average particle spacing is 9.2-9.5 nm. In hypoxic liver, the junctional particles form regular hexagonal packings in which the average center-to-center particle spacing is approximately 8.5 nm. In liver perfused with hypertonic sucrose-calcium solutions, following EDTA solutions, most junctions are pulled apart. The separated junctional membranes, expected to be highly impermeable, contain particles regularly and tightly packed as in hypoxic or DNP-treated junctions. Preliminary measurements indicate also a possible change in particle diameter, from approximately 8.6 nm (control) to approximately 7.7 nm (treated). The structural changes are similar to those previously reported in crayfish and may reflect conformational changes in particle subunits resulting in functional uncoupling.

Adenosine Triphosphate↗

PubMed2005

Adjusting resonance wavelengths of long-period fiber gratings by the glass-structure change.

Long-period fiber gratings written by arc discharge are heated at different temperatures, and the postheating changes of transmission characteristics are investigated. The resonance wavelengths are shifted to longer wavelengths by heating at a temperature lower than the fictive temperature of the fiber, and they move more quickly with increasing heating temperature. The resonance wavelength shifts more for the loss peak generated by the higher cladding mode. It is shown that the resonance wavelengths can be changed and adjusted up to 63-76 nm without significant degradation by the glass-structure change induced by heating.

Journal Article↗

PubMed1999

Structural changes in the transition state of protein folding: alternative interpretations of curved chevron plots.

The interpretation of folding rates is often rationalized within the context of transition state theory. This means that the reaction rate is linked to an activation barrier, the height of which is determined by the free energy difference between a ground state (the starting point) and an apparent transition state. Changes in the folding kinetics are thus caused by effects on either the ground state, the transition state, or both. However, structural changes of the transition state are rarely discussed in connection with experimental data, and kinetic anomalies are commonly ascribed to ground state effects alone, e.g., depletion or accumulation of structural intermediates upon addition of denaturant. In this study, we present kinetic data which are best described by transition state changes. We also show that ground state effects and transition state effects are in general difficult to distinguish kinetically. The analysis is based on the structurally homologous proteins U1A and S6. Both proteins display two-state behavior, but there is a marked difference in their kinetics. S6 exhibits a classical V-shaped chevron plot (log observed rate constant vs denaturant concentration), whereas U1A's chevron plot is symmetrically curved, like an inverted bell curve. However, S6 is readily mutated to display U1A-like kinetics. The seemingly drastic effects of these mutations are readily ascribed to transition state movements where large kinetic differences result from relatively small alterations of a common free energy profile and broad activation barriers.

Amino Acid Sequence↗

PubMed1995

The mechanism of force generation in myosin: a disorder-to-order transition, coupled to internal structural changes.

We propose a molecular mechanism of force generation in muscle, based primarily on site-specific spectroscopic probe studies of myosin heads in contracting muscle fibers and myofibrils. Electron paramagnetic resonance (EPR) and time-resolved phosphorescence anisotropy (TPA) of probes attached to SH1 (Cys 707, in the catalytic domain of the head) have consistently shown that most myosin heads in contracting muscle are dynamically disordered, undergoing large-amplitude rotations in the microsecond time range. Some of these disordered heads are bound to actin, especially in the early (weak-binding, preforce) phase of the ATPase cycle. The small ordered population (10-20%) is rigidly oriented precisely as in rigor, with no other distinct angle observed in contraction or in the presence of intermediate states trapped by nucleotide analogs. These results are not consistent with the classical model in which the entire head undergoes a 45 degree transition between two distinct orientations. Therefore, it has been proposed that the catalytic domain of the myosin head has only one stereospecific (rigor-like) actin-binding angle, and that the head's internal structure changes during force generation, causing the distal light-chain-binding domain to rotate. To test this model, we have performed EPR and TPA studies of probes attached to regulatory light chains (RLCs) in rabbit and scallop myofibrils and fibers. The RLC results confirm the predominance of dynamic (microsecond) rotational disorder in both relaxation and contraction, and show that the different mechanisms of calcium regulation in the two muscles produce different rotational dynamics. In rabbit myofibrils, RLC probes are more dynamically disordered than SH1 probes, especially in rigor and contraction,indicating that the light-chain-binding domain undergoes rotational motions relative to the catalytic domain when myosin heads interact with actin. An SH1-bound spin label, which is sensitive to myosin's internal dynamics, resolves three distinct conformations during contraction, and time-resolved EPR shows that these transitions are coupled to specific steps in the ATPase cycle. We propose that force is generated during contraction by a disorder-to-order transition, in which myosin heads first attach weakly to actin in a nonstereospecific mode characterized by large-scale dynamic disorder, then undergo at least two conformational transitions involving large-scale structural (rotational) changes within the head, culminating in a highly ordered strong-binding state that bears force.

Adenosine Triphosphate↗

PubMed2005

ATP-induced structural change of dephosphocoenzyme A kinase from Thermus thermophilus HB8.

Dephosphocoenzyme A kinase (DCK) catalyzes phosphorylation in the final step of coenzyme A (CoA) biosynthesis. In this phosphorylation process, domain movements play a very important role. To reveal the structural changes induced by ligand binding, we determined the crystal structure of DCK from Thermus thermophilus HB8 by the multiwavelength anomalous dispersion method at 2.8 A. The crystal structure includes three independent protein molecules in the asymmetric unit: One is a liganded form and the others are unliganded. The topology shows a canonical nucleotide-binding protein possessing the P-loop motif. A structure homology search by DALI revealed the similarity of the DCKs from T. thermophilus HB8, Haemophilus influenzae, and Escherichia coli. Structural comparisons between the liganded and unliganded forms of DCK from T. thermophilus HB8 indicated domain movements induced by adenosine triphosphate (ATP) binding. For the domain movements, proline residues confer flexibility at the domain linkages. In particular, Pro91 plays an important role in moving the CoA domain.

Adenosine Triphosphate↗

PubMed1992

Structural changes in condylar cartilage following prolonged exposure to the human parathyroid hormone fragment (hPTH) 1-34 in vitro.

This investigation presents the structural changes in condylar cartilage incubated in the presence of human parathyroid hormone (1-34) in an organ culture system for 6 to 12 days. Control cultures maintained their cartilaginous characteristics whereas human parathyroid hormone (1-34)-treated cultures revealed the following modifications: (1) The chondroprogenitor cell zone at the apical region of the explant underwent a substantial enlargement. The cells changed from a mesenchyme-like morphology into polygonal, glycogen-rich cells that were tightly attached to each other by a fibrillar intercellular matrix, but even by 12 days the apical region was comprised of healthy cells. (2) The mineralizing zone in the hypertrophic cartilage revealed a change in its cellular population. Hypertrophic chondrocytes were replaced by cells with amoeboid extensions and large numbers of secretory granules or vesicles. Based upon the above findings it appears that the chondroprogenitor cells that are initially stimulated to proliferate, are being suppressed from subsequent differentiation into chondroblasts; and that hypertrophic chondrocytes apparently undergo a dedifferentiation process followed by development into an as yet unknown cell population.

Animals↗

PubMed1999

Studies on structural changes of the carotid arteries and the heart in asymptomatic renal transplant recipients.

BACKGROUND: The present study was designed to characterize early structural changes of large arteries in renal transplant recipients with no clinical evidence of cardiovascular disease and normal blood pressure values, and to analyse the relationship between arterial alterations and those of the heart. METHODS: Intima media thickness and atherosclerotic plaques of the carotid arteries as well as left ventricular geometry and function were examined in 35 asymtomatic renal transplant recipients and 29 age- and sex-matched healthy controls by high resolution B-mode ultrasound and by echocardiography. RESULTS: Intima-media thickness of the carotid arteries was significantly higher in renal transplant recipients (1.21+/-0.08 mm) than in healthy controls (0.74+/-0.04 mm) (P<0.001). Atherosclerotic plaques were found in the majority of renal transplant recipients (71% vs 14% in healthy controls, P<0.001). Left ventricular mass index was significantly increased in the group of renal transplant recipients (264+/-13 g, 146+/-7 g/m2) when compared with healthy controls (155+/-8 g, 83+/-4 g/m2) (P<0.001). Multiple regression analysis in renal transplant recipients showed that intima media thickness of the carotid arteries was significantly related to left ventricular mass index (P<0.02), but not to age, blood pressure, body mass index, serum creatinine, cholesterol and lipoprotein (a) levels. In the group of healthy controls, intima-media thickness of the carotid artery was related to age (P<0.002), but not to left ventricular mass index or the other independent variables. CONCLUSIONS: The present study documents pronounced intima-media thickening in asymptomatic renal transplant recipients. Atherosclerotic lesions are present in most renal transplant recipients with no clinical evidence of cardiovascular disease. We observed a parallelism between arterial wall thickening and left ventricular hypertrophy, although blood pressure levels were normal during haemodialysis therapy and after renal transplantation.

Adult↗

PubMed1988

Structural changes in the mouse heart one year after brain exposure to 60Co gamma ray.

This study was conducted to investigate the sequential structural changes in the hearts of C3H male mice 1 to 12 months after brain irradiation. A single brain dose of 8 or 20 60Co gamma Gy was given to the animals at 4 months of age. Degenerative changes in the heart occurred, firstly at 6 months after irradiation, and became progressively more severe at 12 months. The cardiac muscle showed areas of focal myofibrillolysis, myofibrillar degeneration with loss of entire myofibrils, the presence of lysosomal-like bodies, and interstitial fibrosis. Coronary artery degeneration was also found at 12 months after irradiation; the major changes included smooth muscle degeneration with fibrosis, and the accumulation of debris and extracellular matrix. Quantitative analysis indicated that the degeneration of the arterial smooth muscle after 20 Gy irradiation (18.9%) was significantly higher than that of the unirradiated control (13.2%), and shammed control (13.3%) groups, p less than 0.05.

Animals↗