Primary Site Of Injury Research Articles

A 5-Year-Old Girl With Impaired Renal Function After Autologous Bone Marrow Transplantation

ONE MARROW TRANSPLANTATION(BMT) increasingly is used for the treatmentof patients with hematologic malignancies, somemetabolic and immunologic diseases, and de-pressed bone marrow after cancer treatment. Renalinsufficiency after BMT is common and related tomanycauses.Wepresentthecaseofagirlwhohadrenalinsufficiency4monthsafterautologousBMT.

Increased thalamic neurodegeneration following ischaemic cortical stroke in osteopontin-deficient mice

Inflammation aggravates brain injury caused by stroke and neurodegeneration. Osteopontin (OPN) is a cytokine-like glycoprotein that binds to various integrins and CD44 variants. OPN exerts proinflammatory effects in autoimmune conditions but also has cytoprotective properties and participates in wound healing. In this study, we addressed the role of OPN in ischaemic brain injury using OPN knock-out (KO) mice in models of cortical stroke. Compared with wild-type animals, OPN KO mice exhibited unaltered infarct development at the primary injury site but greatly increased retrograde degeneration of the ipsilateral thalamus. Thalamic neurodegeneration in OPN-deficient mice was associated with pronounced microglia activation and inflammatory gene expression and could be attenuated via pharmacological blockade of the inducible nitric oxide synthase (iNOS). Therefore, delayed neurodegeneration in OPN-deficient mice was at least partly due to an excessive release of nitric oxide via the iNOS pathway. Neuroprotective and anti-inflammatory effects of OPN may be relevant for a variety of neurological disease conditions.

Tightly regulated distribution of family members of proteins is related to social property in the open body system (Review)

Environmentally mediated systemic involvement of autoimmunity, allergy and carcinogenesis are very common by clinical and epidemiological investigation. However, there is an unknown relationship between environment and environmentally mediated systemic involvement of autoimmunity, allergy and carcinogenesis. This unknown molecular communication or response conducts the primary injury sites of the skin, and surface mucosa in the respiratory, alimentary, or reproductive tracts, to the secondary sites or even the whole body under some physiological and pathological conditions. Also, this unknown molecular communication or response involves a variety of molecular events, detectable in systemic differentiation, overexpression, hyperplasia, carcinogenesis, allergies or autoimmunity. The family members of proteins and their relatives are almost ubiquitous, and distribution is tightly regulated at all three administrative levels to form an interacting multiprotein complex. The key question is whether there is unknown communication or response among the family members and, if there is, is it associated with some social property of the proteins in the open body system?

Scleral edge, not optic disc or retina, is the primary site of injury in chronic glaucoma

In chronic glaucoma, there is a gradual painless loss of vision, early manifestation of arcuate field defect and typical atrophy of the optic disc known as 'cupping'. Chronic glaucoma is classified into high-tension glaucoma (HTG) and normal-tension glaucoma (NTG). Although both types manifest with the same typical visual field defect and cupping of the optic disc, high-tension glaucoma has elevated intraocular pressure whereas in normal-tension glaucoma the intraocular pressure (IOP) is within the normal range (10-21 mmHg). There are several theories about the pathogenesis of chronic glaucoma ranging from high intraocular pressure directly damaging the optic disc to programmed death(apoptosis) of the ganglion cells of the retina. But none of them satisfactorily explain the manifestation of the early arcuate field defect which is a pathognomonic feature of both types of chronic glaucoma. This article focuses on two main issues. First, how and why the arcuate field defects are produced in the early stages of glaucoma and secondly to find out the common ground in the pathogenesis of both high and normal tension glaucoma. The early arcuate field defects are an important lead in discovering the pathogenesis of glaucoma, therefore if any factor or site which could not possibly produce initial sharply defined arcuate field defects was ruled out. This article presents an unconventional approach to the pathogenesis of glaucoma. Instead of looking for various factors causing glaucoma, emphasis was placed on determining the primary site of injury which could produce the initial arcuate field defects. Keeping the arcuate visual field defects in mind, the primary site of injury appears to be at the scleral edge and not the optic disc or the retina in chronic glaucoma. The border tissue which separates the sclera and choroid from the nerve fibers would atrophy due to chronic ischemia as a result of high intraocular pressure in HTG, whereas due to poor systemic circulation in NTG. In both types of chronic glaucoma, the ciliary circulation supplying the prelaminar and border tissue is compromised. As a result of atrophy of the border tissue, the optic disc sinks as a whole beginning temporally due to its tilted position and causing nerve fibers to stretch, kink, and cut at the scleral edge. This process of optic disc sinking would accelerate due to loss of nerve fibers which also provides anchorage to the optic disc. This cycle would continue until all the nerve fibers are cut at the scleral edge and the optic disc is destroyed.

Plasticity of Mesangial Cells: A Basis for Understanding Pathological Alterations

In the last two decades, the ability of mesangial cells to respond to various stimuli or injurious agents by altering their phenotype and function has become recognized. The plasticity of these mesangial cells has been linked to the morphological and functional alterations responsible for the pathologic findings. Many of the glomerular disorders target the mesangium as the primary and/or initial site of injury. Understanding how mesangial cells are altered in the various conditions provides a platform for conceptualizing pathologic mechanisms and defining key steps amenable to therapeutic intervention. The present paper reviews the normal and altered mesangium with an emphasis on mechanisms involved in alterations of mesangial homeostasis. Mesangial cells and matrix are very important in maintaining normal glomerular structure, and function and the plasticity of these cells is responsible for pathological manifestations, repair, and scarring. Our more sophisticated understanding of mesangial cell behavior and matrix biology provides very useful information to help design new therapeutic approaches to the treatment of renal diseases. The potential for bone marrow-derived cells to differentiate into mesangial cells and repopulate damaged mesangium, thus “healing” what is today considered to be irreversible damage represents an exciting new area of research.

Altered Gene Expression Profiles Reveal Similarities and Differences Between Parkinson Disease and Model Systems

Parkinson disease (PD) targets dopaminergic neurons in the substantia nigra, resulting in motor disturbances such as resting tremor, bradykinesia, and rigidity. Pathogenic processes likely occur over several decades, in that an overwhelming percentage of neurons are already dead at the time of clinical diagnosis. For this reason, the usage of animal model systems to discover the early steps in the pathologic cascade is required. These include exposure to the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), which selectively kills dopamine neurons in the substantia nigra, and genetic models incorporating mutations in the α-synuclein gene that cause disease in human patients. Through the evaluation of these models at multiple time points, it is possible to discover novel gene expression changes that may underlie disease pathogenesis. Specifically, the authors hypothesize that animal models of PD and human PD brains share a gene expression profile that signifies certain aspects of pathogenesis and/or recovery-resistance. To test this and similar hypotheses, the authors and others have utilized new microarray technology that enables the sampling of thousands of genes’ expression level in one assay. Because the technology is fairly new and results can vary depending on methods used, results must be evaluated with care. Multiple array and data-mining options can be used to make the most accurate inferences as to differentially expressed genes in each set of samples. The authors developed a fusion classifier approach whereby individual data-mining algorithms generate lists of significant genes. The lists are subsequently queried, and only genes unanimously called significant are retained for further validation. Although the authors’ approach identified hundreds of differentially expressed genes in each of three PD systems, only a few were common between the human and animal substantia nigra. These were related to dopamine phenotype, synaptic function, and the mitochondrial metabolism, implicating the presynaptic terminal as a primary site of injury. The time course of the authors’ experiments indicates that if the synaptic changes could be prevented, this may alleviate some cell death, in that these changes precede neuronal loss.

Responses of the plasma membrane to low temperatures

The plasma membrane is considered to be the primary site of injury when plant cells are subjected to extracellular freezing. In order for plants or plant cells to acquire freezing tolerance, it is, thus, necessary that the plasma membrane increases its cryostability during freeze‐thaw excursion. During cold acclimation both under natural and artificial conditions, there are compositional, structural and functional changes occurring in the plasma membrane, many, if not all, of which ultimately contribute to increased stability of the plasma membrane under freezing conditions. In addition, changes in the cytosol or intracellular compartments also affect the cryobehaviour of the plasma membrane during freeze‐induced dehydration. Although many alterations occurring during cold acclimation influence the cryobehaviour of the plasma membrane comprehensively, recent advances in functional genomics approaches provide interesting information on the function of specific proteins for plasma membrane behaviour under freezing conditions.

Osteopontin mediates neuroprotection via inhibition of inducible nitric oxide synthase

Neurodegeneration following ischemic stroke extends from the ischemic infarct to nonischemic subcortical regions such as the ipsilateral thalamus. At both sites, inflammation with activation of resident microglia/brain macrophage ensues and may exacerbate the degenerative process. Osteopontin (OPN) is a macrophage-derived secreted glycoprotein with cytokine-like and chemoattractant properties mediated via RGD-binding integrin receptors and CD44. OPN exerts proinflammatory effects in autoimmune conditions, but also participates in beneficial wound healing responses. Here, we addressed the role of OPN in ischemic brain injury using OPN knock-out (KO) mice in models of cortical stroke. Compared to wild-type (WT) animals, OPN KO mice exhibited unaltered infarct development at the primary injury site but greatly increased secondary neurodegeneration of the ipsilateral thalamus. Thalamic neurodegeneration in OPN-deficient mice was associated with excessive microglia activation and inflammatory gene expression and could be attenuated via pharmacologic blockade of the inducible nitric oxide synthase (iNOS). Thus, OPN provided neuroprotection through down-regulation of microglia activation and iNOS. OPN-dependent pathways may represent a new target of neuroprotective therapy in neurodegenerative diseases and stroke.

Restoration of Cerebral Vasoreactivity by an L-Type Calcium Channel Blocker following Fluid Percussion Brain Injury

Traumatic brain injury (TBI) results in significant acute reductions in regional cerebral blood flow (rCBF). However, the mechanisms by which TBI impairs CBF and cerebral vascular reactivity have remained elusive. In the present study, the effect of verapamil, an L-type calcium (Ca(2+)) channel blocker, on post-traumatic vascular reactivity was evaluated following a lateral fluid percussion injury (FPI) in rats. rCBF was measured by [(14)C]-iodoantipyrine autoradiography 1 h after FPI. Following FPI, significant rCBF reductions were documented in all examined cortical areas. These reductions were the most prominent (72.0%) at the primary injury site. Intravenous infusion of verapamil (VE; 200 microg/kg/min), and norepinephrine (NE; 20 microg/mL/min) to maintain normal blood pressure, increased rCBF by 141.5% at the primary injury site when compared to untreated, FPinjured animals. Under stimulated conditions, both the ipsilateral and contralateral hemispheres failed to show any increases in rCBF at 1 h following FPI. In direct contrast, following VE+NE treatment all cortical areas measured showed near normal vascular reactivity to direct cortical stimulation (normal reactivity = 45% increase in rCBF vs. 47% increase in FPI+VE+NE cases). These findings suggest that the majority of post-traumatic hemodynamic depressions are closely related to mechanisms involving vasoconstriction. Furthermore, Ca(2+) may play a causative role in this vasoconstriction and the loss of vasoreactivity.

Neonatal Hemochromatosis: Is It an Alloimmune Disease?

Neonatal hemochromatosis (NH) has been defined clinically as severe neonatal liver disease in association with extrahepatic siderosis in a distribution similar to that seen in HFE-associated hereditary hemochromatosis (1). Though it is generally considered a rare disease, it is one of the most commonly recognized causes of liver failure in the neonate and a frequent indication for liver transplantation in the first 3 months of life (2–4). Its etiology and pathogenesis are as yet unknown. Indeed, it has been considered to be a syndrome in which a number of primary etiologies, such as infection, genetic-metabolic disease and toxic insult, lead to a common phenotype. We have hypothesized that much, if not all, NH is a consequence of gestational alloimmune disease. This review presents the clinical evidence leading to this hypothesis, the data we have collected in its support, and the direction our investigations are taking to ultimately prove or disprove it.

Retinal ganglion cell apoptosis in glaucoma is related to intraocular pressure and IOP-induced effects on extracellular matrix.

To investigate the effect of IOP on retinal ganglion cell (RGC) apoptosis and correlate the effects with IOP-induced changes in extracellular matrix (ECM) in the retina and optic nerve head (ONH) in glaucomatous rat eyes. Thirty-seven Dark Agouti rats had elevated IOP induced in the left eye by hypertonic saline episcleral vein injections. Eyes were examined at 3 months histologically for RGC apoptosis and expression of specific ECM components. RGC apoptosis was significantly related to IOP exposure (integral DeltaIOP P <0.001; peak IOP P <0.01). In the RGC layer, elevated IOP correlated positively to a significant increase in MMP-9 activity (P <0.001), tissue inhibitor of matrix metalloproteinase (TIMP-1) (P <0.05), and collagen I (P <0.01), and negatively correlated to deposition of laminin (P <0.05) and TGF-beta2 (P <0.05). There was a significant correlation between MMP-9 activity and both RGC apoptosis (P <0.001) and loss of laminin (P <0.01). IOP exposure was also associated with increased deposition of TGF-beta2 and collagen I at the ONH (P <0.01). The results demonstrated that RGC apoptosis in glaucoma correlates strongly with elevated IOP and is significantly associated with IOP-induced changes in specific ECM components in the RGC layer. The study shows for the first time a link between MMP-9, laminin degradation, RGC apoptosis, and IOP exposure in glaucoma. The findings suggest that abnormal ECM remodeling in the glaucomatous retina may relate to RGC death and support the notion that the retina is a primary site of injury in glaucoma.

Electromyographic and kinematic exploration of whiplash-type rear impacts: effect of left offset impact

Background context Although there are some volunteer collision studies reporting the effects of rear impacts on head and neck kinematics, there are few studies detailing the cervical muscle electromyogram response. Moreover, the effect of a rear impact offset to the left on the resultant muscle responses is unknown. Purpose The purpose of this study was to determine the response of the cervical muscles to increasing low-velocity rear impacts offset by 45 degrees to the subject's left, and to compare the quantitative effects of expected and unexpected impact. Study design/Setting Nine healthy volunteers were subjected to rear impacts, offset by 45 degrees to the subject's left, of 4.6, 8.7, 11.0 and 14.5 m/s 2 acceleration, at two levels of expectation: expected and unexpected. Methods Bilateral electromyograms of the sternocleidomastoids, trapezii and splenii capitis were recorded. Triaxial accelerometers recorded the acceleration of the chair, torso at the shoulder level and head of the participant. Results At an acceleration of 14.5 m/s 2, the left sternocleidomastoid generated 71% and the right sternocleidomastoid 82% of their maximal voluntary contraction electromyogram in the unexpected impact conditions. Under these conditions, the right splenius capitis (contralateral to the left offset rear impact) also generated 71% of its maximal voluntary contraction, whereas the left splenius capitis generated only 20% of this variable. The trapezii generated only 25% of their maximal voluntary contraction. Subjects exhibited lower levels of their maximal voluntary contraction electromyogram when the impact was expected. Electromyographic variables were significantly affected by the levels of acceleration and expectation (p<.001). The time to onset and time to peak electromyogram for all muscles progressively decreased with increasing levels of acceleration, in the unexpected condition. The kinetic variables and the electromyographic variables regressed significantly on the acceleration (p<.001). In response to rear impacts offset to the subject's left, muscle responses were greater with higher levels of acceleration, greater with unexpected impact conditions and greatest for both sternocleidomastoids and for the splenius capitis muscle contralateral to the side of impact. Conclusions Because the muscular component of the head-neck complex plays a role in the abatement of impact at higher acceleration levels, they are likely a primary site of injury in the whiplash phenomenon in rear collisions. More specifically, when a rear impact is offset to the subject's left, it results in not only increased electromyographic generation in both sternocleidomastoids, but the splenius capitis contralateral to the direction of impact offset also bears part of the force of the neck perturbation. Expecting or being aware of imminent impact also plays a role in reducing muscle responses in low-velocity offset rear impacts.

Cervical Muscle Response to Whiplash-Type Right Lateral Impacts

Nine healthy volunteers were subjected to right lateral impacts of 4.9, 8.8, 10.8, and 13.7 m/sec acceleration at two levels of expectation: expected and unexpected. To determine the response of the cervical muscles to increasing low-velocity right lateral impacts and compare the quantitative effects of expected and unexpected impact. The literature contains little information on the etiology of whiplash injuries. In particular, in vivo studies of the cervical muscular response and head-neck kinematics to lateral impacts are rare. A previous study of left lateral impacts suggests that the burden of impact is borne primarily by the muscles contralateral to the side of impact. Bilateral electromyograms of the sternocleidomastoids, trapezii, and splenii capitis were recorded. Triaxial accelerometers recorded the acceleration of the chair, torso at the shoulder level, and head of the participant. At an acceleration of 13.7 m/sec2, both sternocleidomastoids, both trapezii, and the right splenius capitis generated on average around 40% or less of their maximal voluntary contraction electromyogram in both the expected and unexpected impact conditions. The left splenius capitis (i.e., contralateral to the right lateral impact), however, generated 84% of its maximal voluntary contraction electromyogram (double the response of other muscles). Electromyographic variables were affected significantly by the levels of acceleration (P < 0.01). The time to onset and time to peak electromyogram time for all muscles decreased progressively with increasing levels of acceleration. The kinetic variables and the electromyographic variables regressed significantly on the acceleration (P < 0.01), and the head acceleration was affected significantly by expectation (P < 0.01). In response to right lateral impacts, muscle responses were generally greater, with higher levels of acceleration, and greatest for the splenius capitis muscle contralateral to the side of impact (P < 0.01). Because the muscular component of the head-neck complex likely plays a central role in the abatement of higher acceleration levels, it may be a primary site of injury in the whiplash phenomenon in lateral collisions, and specifically, the splenius capitis muscle contralateral to the side of impact is most likely to be injured. Being aware of an impact may reduce the degree of head perturbation.

Electromyographic and kinematic exploration of whiplash-type left anterolateral impacts.

Volunteer studies of the cervical muscular response and head-neck kinematics in response to frontal impacts are uncommon. Moreover, the effect of a frontal impact offset to the left on the resultant muscle responses is unknown. The purpose of this study was to determine the response of the cervical muscles to increasing low-velocity frontal impacts offset by 45 degrees to the left and to compare the quantitative effects of expected and unexpected impact. Nine healthy volunteers were subjected to frontal impacts, offset by 45 degrees to the subject's left, of 5.0, 8.7, 11.3, and 15.6 m/s2 of acceleration at two levels of expectation: expected and unexpected. Bilateral electromyograms (EMGs) of the sternocleidomastoids, trapezii, and splenii capitis were recorded. Triaxial accelerometers recorded the acceleration of the chair, torso at the shoulder level, and head of the participant. Subjects tended to exhibit lower percentages of their maximal voluntary contraction EMG when the impact was expected. When the impact was unexpected, and at an acceleration of 15.6 m/s2, the splenius capitis muscle contralateral to the impact (ie, right splenius in a left anterolateral impact) generated 95% of its maximal voluntary contraction EMG, whereas the left splenius (ipsilateral to the left anterolateral impact) generated only 43% of this variable. Under these same conditions, the trapezii responded symmetrically, generating approximately 80% of their maximal voluntary contraction EMG. At an acceleration of 15.6 m/s2, the sternocleidomastoids generated approximately 37% of their maximal voluntary contraction EMG in both the expected and the unexpected impact conditions. EMG (such as time to peak EMG) and kinematic variables were significantly affected by the levels of acceleration (P < 0.001) and expectation status (P < 0.05). The time to onset of the EMG for the splenii capitis and trapezii progressively decreased with increasing levels of acceleration. In response to left anterolateral impacts, muscle responses were greater with higher levels of acceleration and greatest for the splenius capitis muscle contralateral to the side of impact. The head acceleration response was greater in the unexpected than in the expected condition (P < 0.05). Because the muscular component of the head-neck complex plays a central role in the abatement of higher acceleration levels, this is likely a primary site of injury in the whiplash phenomenon in frontal collisions. More specifically, when a frontal impact is offset to the subject's left, it not only results in increased EMG generation in both trapezii, but the splenius capitis contralateral to the direction of impact also bears part of the force of the neck perturbation. Expecting or being aware of imminent impact may play a role in reducing muscle responses in low-velocity anterolateral impacts.

Crush injury induces NMDA-receptor-dependent delayed nerve cell death in rat entorhinal–hippocampal slice cultures

The aim of the present study was to develop an in vitro model that produces an injury-induced delayed nerve cell death. We used entorhinal–hippocampal slices from 12-day-old rats, which were cultured for 14 days before experiments prior to a crush injury in the middle layers of the entorhinal cortex. Crush injury increased specific propidium iodide (PI) fluorescence at the site of primary injury at day 1. Specific PI fluorescence decreased over the following days, with a slower decrease taking place at days 4–7. At days 4–7, PI fluorescence increased in CA1 and CA3. Treatment with 30 μM MK-801 for 2 h at the time of crush injury prevented the increase in PI fluorescence at days 4–7 at the site of injury, in CA1, and in CA3. Crush injury induced TUNEL-positive cells at the site of injury at days 1 and 5. MK-801 markedly reduced the number of TUNEL-positive cells observed at day 5, but had no effect on the number of TUNEL-positive cells at day 1. The present data indicate that crush injury may induce two types of secondary cell death. The first, early, type of cell death is induced quickly and is maximal at day 1, after which the dead cells are gradually removed. The second, delayed, type of cell death appears at day 4. NMDA receptor antagonism prevents the induction of the delayed cell death but has no effect on the early cell death.

Regularity of distribution of immunoreactive pulmonary surfactant protein A in rat tissues

Existing data has shown that SP-A-like protein or mRNA is widely distributed in lamellar bodies such as tissues and mucosal surfaces. Using immunohistochemistry method with a polyclonal antibody against human SP-A, in this study we investigated distribution of immunoreactive pulmonary surfactant protein A (IR-SP-A) in a number of rat tissues. The SP-A-like immunoreactivity was found in alveolar, parenchyma, pleura of lung; myelin sheath of brain; epithelia of Bowman's capsule, glomerulus and renal tubules of kidney; epithelia of colon, stomach, duct of salivary gland, pharynx; and blood vessel wall and connective tissue of extracellular matrix. The positive signal was blocked by pre-absorbed SP-A antigen from recombinant or bronchoalveolar lavage (BAL). SP-A has long been considered as an important frontier host defense molecule which participates in immune and inflammatory regulation of lung. With every inhalation, small particles, viruses, bacteria, and antigens from environment are continuously deposited onto the vast pulmonary epithelial surface. While a proper host defense is required to protect the lung, an over-exuberant response can disrupt the appropriate balance between pro- and anti-inflammatory. Traditional Chinese medicine believes that body is an open system relevant to the external environment. The physical, chemical and biological environmental factors constantly affect the open system, and the body properly reacts to maintain homeostasis of body machinery. The Chinese traditional medicine scholars have thus hypothesized that 'Qi' (meaning air) is the communication way between the body and external environment. What is 'Qi'? The results from our study suggest that IR-SP-A is a candidate of 'Qi'. It is compatible with the sites, theoretically containing collagenous and lectin domain molecules, also compatible with the primary injury sites of some autoimmune diseases. SP-A may be as one of 'Qi' molecules mentioned in traditional Chinese medicine that trigger some of autoimmune diseases.

Prior Injuries &amp; Future Participation in National Football League (NFL) Prospects

2215 PURPOSE & METHODS: To analyze sports medicine injuries and to predict future participation in the National Football League, we evaluated medical, physical, and performance variables in 384 (196 Offense, 149 Defense, and 39 Undefined) top US college football players who were tested at the 2000 Indianapolis NFL Combine. We then tracked these players' participation in the NFL over the next two consecutive years by using NFL consolidated summaries collected after each pro game. RESULTS: Within the previous 5 yr, 58% (n = 223) of players accounted for 524 significant injuries and 257 surgeries or 1.4 injuries and 0.7 surgeries per player for the entire group. 17% (n = 64) had 1 injury, 18% (n = 70) had 2 injuries, 15% (n = 58) had 3 injuries, and 8% (n = 31) had 4 or more injuries within the past 5 yr. The most recent, primary sites of injury were the knee (20%, n = 77), shoulder (11%, n = 42), ankle (7%, n = 26), lower back (5%, n = 19) and hand (3%, n = 13). The top primary diagnoses were tear (18%, n = 70), dislocation/subluxation (9%, n = 36), fracture (7%, n = 28), and repetitive trauma/loose bodies (7%, n = 26). 14% of players (n = 54) had significant degenerative joint diseases or arthritis as documented by comprehensive orthopedic analyses and imaging. The highest body mass indices (BMI) were in offensive lineman and defensive tackles (both 38), while the lowest were in defensive backs (27) and wide receivers (26). For all player classifications, average BMI were higher than national recommendations (< 25) predicting relatively higher disease risk and a shortened life span. Though there was wide variability, offensive lineman (yr 1: 16%, yr 2: 21%), wide receivers (yr 1: 14%, yr 2: 18%), defensive ends (yr 1: 17%, yr 2: 27%) and linebackers (yr 1: 15%, yr 2: 29%) had the highest participation. 61% of players (n = 235) were classified as minimal participants (<10% of plays for both yr). For offense, orthopedic grade was a significant predictor of participation in running backs (8% of variance) and wide receivers (10% of variance) for the 1st year (both P<0.05). For defense, the total number of injuries (11%) and total number of surgeries (11%) were significant predictors of participation in linebackers only (both P<0.05). CONCLUSIONS: While predicting participation may be crucial from an owner and coach perspective, we are concerned more with the health and well-being of these athletes well into the future. Our data imply that many players who report to the Combine have significant injuries prior to entering the NFL, that a vast majority subsequently drafted have very little impact in the 1st and 2nd yr, and that BMI, preexisting injuries and arthritis predict significant future health consequences.

Prior Injuries &amp; Future Participation in National Football League (NFL) Prospects

2215 PURPOSE & METHODS: To analyze sports medicine injuries and to predict future participation in the National Football League, we evaluated medical, physical, and performance variables in 384 (196 Offense, 149 Defense, and 39 Undefined) top US college football players who were tested at the 2000 Indianapolis NFL Combine. We then tracked these players' participation in the NFL over the next two consecutive years by using NFL consolidated summaries collected after each pro game. RESULTS: Within the previous 5 yr, 58% (n = 223) of players accounted for 524 significant injuries and 257 surgeries or 1.4 injuries and 0.7 surgeries per player for the entire group. 17% (n = 64) had 1 injury, 18% (n = 70) had 2 injuries, 15% (n = 58) had 3 injuries, and 8% (n = 31) had 4 or more injuries within the past 5 yr. The most recent, primary sites of injury were the knee (20%, n = 77), shoulder (11%, n = 42), ankle (7%, n = 26), lower back (5%, n = 19) and hand (3%, n = 13). The top primary diagnoses were tear (18%, n = 70), dislocation/subluxation (9%, n = 36), fracture (7%, n = 28), and repetitive trauma/loose bodies (7%, n = 26). 14% of players (n = 54) had significant degenerative joint diseases or arthritis as documented by comprehensive orthopedic analyses and imaging. The highest body mass indices (BMI) were in offensive lineman and defensive tackles (both 38), while the lowest were in defensive backs (27) and wide receivers (26). For all player classifications, average BMI were higher than national recommendations (< 25) predicting relatively higher disease risk and a shortened life span. Though there was wide variability, offensive lineman (yr 1: 16%, yr 2: 21%), wide receivers (yr 1: 14%, yr 2: 18%), defensive ends (yr 1: 17%, yr 2: 27%) and linebackers (yr 1: 15%, yr 2: 29%) had the highest participation. 61% of players (n = 235) were classified as minimal participants (<10% of plays for both yr). For offense, orthopedic grade was a significant predictor of participation in running backs (8% of variance) and wide receivers (10% of variance) for the 1st year (both P<0.05). For defense, the total number of injuries (11%) and total number of surgeries (11%) were significant predictors of participation in linebackers only (both P<0.05). CONCLUSIONS: While predicting participation may be crucial from an owner and coach perspective, we are concerned more with the health and well-being of these athletes well into the future. Our data imply that many players who report to the Combine have significant injuries prior to entering the NFL, that a vast majority subsequently drafted have very little impact in the 1st and 2nd yr, and that BMI, preexisting injuries and arthritis predict significant future health consequences.

Electron transport is the functional limitation of photosynthesis in field‐grown Pima cotton plants at high temperature

ABSTRACTRestrictions to photosynthesis can limit plant growth at high temperature in a variety of ways. In addition to increasing photorespiration, moderately high temperatures (35–42 °C) can cause direct injury to the photosynthetic apparatus. Both carbon metabolism and thylakoid reactions have been suggested as the primary site of injury at these temperatures. In the present study this issue was addressed by first characterizing leaf temperature dynamics in Pima cotton (Gossypium barbadense) grown under irrigation in the US desert south‐west. It was found that cotton leaves repeatedly reached temperatures above 40 °C and could fluctuate as much as 8 or 10 °C in a matter of seconds. Laboratory studies revealed a maximum photosynthetic rate at 30–33 °C that declined by 22% at 45 °C. The majority of the inhibition persisted upon return to 30 °C. The mechanism of this limitation was assessed by measuring the response of photosynthesis to CO2 in the laboratory. The first time a cotton leaf (grown at 30 °C) was exposed to 45 °C, photosynthetic electron transport was stimulated (at high CO2) because of an increased flux through the photorespiratory pathway. However, upon cooling back to 30 °C, photosynthetic electron transport was inhibited and fell substantially below the level measured before the heat treatment. In the field, the response of assimilation (A) to various internal levels of CO2 (Ci) revealed that photosynthesis was limited by ribulose‐1,5‐bisphosphate (RuBP) regeneration at normal levels of CO2 (presumably because of limitations in thylakoid reactions needed to support RuBP regeneration). There was no evidence of a ribulose‐1,5‐bisphosphate carboxylase/oxygenase (Rubisco) limitation at air levels of CO2 and at no point on any of 30 A–Ci curves measured on leaves at temperatures from 28 to 39 °C was RuBP regeneration capacity measured to be in substantial excess of the capacity of Rubisco to use RuBP. It is therefore concluded that photosynthesis in field‐grown Pima cotton leaves is functionally limited by photosynthetic electron transport and RuBP regeneration capacity, not Rubisco activity.

Electromyographic and Kinematic Exploration of Whiplash-Type Neck Perturbations in Left Lateral Collisions

Seven healthy volunteers were subjected to left lateral impacts of 4.8, 7.9, 11, and 13.7 m/s acceleration at two levels of expectation: expected and unexpected. The purpose of this study was to determine the response of the cervical muscles to increasing low-velocity left lateral impacts, and to compare the quantitative effects of expected and unexpected impact. The literature contains little information on the etiology of whiplash injuries. Animal and cadaver studies have yielded some insight into the phenomenon. However, in vivo studies of the cervical muscular response and head-neck kinematics to lateral impacts are rare. Bilateral electromyograms of the sternocleidomastoids, trapezii, and splenii capitis were recorded bilaterally. Triaxial accelerometers recorded the acceleration of the chair, torso at the shoulder level, and head of the participant. At an acceleration of 13.7 m/s, the sternocleidomastoids and trapezii generated approximately <or=50% of their maximal voluntary contraction electromyogram in both the expected and unexpected impact conditions. Study participants exhibited lower levels of their maximal voluntary contraction electromyogram when the impact was expected. The splenius capitis behaved similar to these muscles in the expected condition, but when the impact was unexpected, the splenius capitis muscle contralateral to the impact (i.e., right splenius in a left lateral impact) generated 94% of its maximal voluntary contraction electromyogram. Electromyographic variables were significantly affected by the levels of acceleration and expectation (P < 0.001). The onset time and peak electromyogram time for the sternocleidomastoid, splenii capitis, and trapezii on the side contralateral to the side of impact progressively decreased with increasing levels of acceleration. The onset time and peak electromyogram time for the sternocleidomastoid, splenii, and trapezii on the same side of impact progressively increased with increasing levels of acceleration. The kinetic variables and the electromyographic variables regressed significantly on the acceleration (P < 0.01). In response to left lateral impacts, muscle responses were greater with higher levels of acceleration, greater with unexpected impact conditions, and greatest for the splenius capitis muscle contralateral to the side of impact. Because the muscular component of the head-neck complex plays a central role in the abatement of higher acceleration levels, it may be a primary site of injury in the whiplash phenomenon in lateral collisions. Expecting or being aware of imminent impact may play a role in reducing muscle responses in low-velocity impacts.