Signs Of Repair Research Articles

Peculiarities of the ST-segment elevation myocardial infarction morphogenesis after mechanical restoration of epicardial blood flow without ECG signs of reperfusion

The aim of the study was to investigate the peculiarities of STEMI morphogenesis after mechanical restoration of epicardial blood flow without ECG signs of reperfusion. The autopsy data of 44 patients with STEMI who died at different times after PCI performed within the first 12 hours (27 cases), or 12–24 hours (17 cases), without ECG signs of reperfusion after the intervention, were analyzed. The comparison group consisted of 85 deceased without reperfusion therapy (RT). Histological examination of the myocardium was performed at following time: within 12 hours, at 13–24 hours, 2–4 days, 5–8 days, 9–15 and 16–22 days. The most common cause of death was acute left ventricular failure (ALVF) both in the group of blood flow restoration without ECG signs of reperfusion, and in the group without RT: 85 % and 79 %, respectively. In each of the two groups the number of deaths occurred in the first 12 hours exceeded one third, half of the patients died in the subsequent 12 hours, two thirds of the deaths occurred within further 2–3 days. The rates of risk factors: older age, anterior and recurrent myocardial infarction, three-vessel lesion of the coronary artery, and a large infarction area were similar in the two groups. From the first hours after PCI, the infarction zone was characterized by hemorrhagic imbibition, numerous injuries of the microcirculatory bed, by the signs of blood flow restoration in damaged vessels appeared from days 2–4, early manifestations of repair from days 5–7. In the MI group without PCI, the hemorrhagic demarcation started on days from 3–4, coagulation necrosis prevailed in the microvascular bed, signs of repair appeared at a later date. Multiple spasms and thromboses in the microvasculature may have been a response to a blood pressure drop that accompanies an acute decrease in the left ventricle contractile function caused by a large infarction area and/or unresolved complications arising during the interventions per se. This mechanism explains the rapid progression of left ventricular failure, the most common cause of death after the interventions with achieving the epicardial blood flow without ECG signs of reperfusion. The revealed microcirculation disorders reflect the absence of myocardial reperfusion, which is more prognostically significant than the restoration of epicardial blood flow.

중복판과 인경본 비교를 통한 고려대장경판 보존관리

The Goryeo Tripitaka woodblocks are the only extant Tripitaka woodblocks carved in Chinese characters, and are included on UNESCO’s Memory of the World Register. 112 of the 81,352 woodblocks that constitute the Goryeo Tripitaka are duplicates a term that refers to woodblocks of which two or more copies exist. 50 of the 112 duplicate woodblocks are thought to be first editions dating from the reign of Goryeo king Gojong (1236~1251); as such, they are highly valuable. These duplicates show various damage due to conservation processes or repeated printing, providing important information about the preservation and repair history of the blocks. In this article, I analyze the current status of duplicate woodblocks and examine the history of their preservation through comparison with printed texts.BR I begin with brief examination of the current status of duplicate woodblocks. The sutra that accounts for the highest number of duplicates is the Prajñāpāramitā Sutra. But since examination of the entire sutra is not possible, I take a sample of 15 blocks and examine them for signs of damage including whether end blocks (maguri) and metal fasteners (jangseok) are present, and whether repairs have been performed. I then examine prints made from these woodblocks, focusing in particular on whether blocks used to make prints in 1381 were still being used in 1865 by gauging the level of similarity between printed copies from each of these two periods.BR I compare the sutra now in the collection of Otani University, which was printed in 1381, with the copies at Woljeongsa Temple and Oseam Hermitage, which were printed in 1865, and with the copies at Tongdosa and Haeinsa temples, printed in 1899. In order to gauge changes that occurred between 1381 and 1865, I analyze all 130 volumes of Prajñāpāramitā Sutra, finding that no changes have occurred. This indicates that the Goryeo Tripitaka woodblocks were fundamentally managed in a stable manner until 1865. However, comparison of printed copies does reveal traces of repair to heavily damaged duplicate blocks. The Woljeongsa and Oseam copies show the following signs of repair in duplicate blocks in places where the original blocks have been worn or their corners damaged: cases where damaged parts have been cut off in order to prevent further damage; cases where repair has been attempted after cutting; cases where repairs have been completed after cutting; and cases where repaired parts have been damaged again after repair. These various examples of repair indicate that such measures were taken continuously throughout the Joseon period, especially after 1865.BR Moreover, examples of supplementary carvings show us that a considerable proportion of duplicate blocks dating from the 1899 prints onwards were supplementary carvings with boundary lines between the columns of characters. I believe these replacement carvings with boundary lines were produced after 1865, in cases where woodblocks that had been repaired were nonetheless deemed unsuitable for printing.

LINGO-1 siRNA nanoparticles promote central remyelination in ethidium bromide-induced demyelination in rats.

Multiple sclerosis is among the most common causes of neurological disabilities in young adults. Over the past decade, several therapeutic strategies have emerged as having potential neuroprotective and neuroregenerative properties. We investigated the effect of intranasal administration of LINGO-1-directed siRNA-loaded chitosan nanoparticles on demyelination and remyelination processes in a rat model of demyelination. Adult male Wistar rats were randomly assigned to one of 6 groups (n= 10 each) and subjected to intrapontine stereotaxic injection of ethidium bromide (EB) to induce demyelination. EB-treated rats were either left untreated or received intranasal LINGO-1-directed siRNA-chitosan nanoparticles from day 1 to day 7 (demyelination group) or from day 7 to day 21 (remyelination group) after EB injection. Chitosan nanoparticle (50μl) was given alone after EB stereotaxic injection for both demyelination and remyelination groups. Two additional groups received 10μl of saline by stereotaxic injection, followed by intranasal saline as controls for demyelination and remyelination groups (n = 10/group). Behavioural testing was conducted for all rats, as well as terminal biochemical assays and pathological examination of pontine tissues were done. After EB injection, rats had compromised motor performance and coordination. Pathological evidence of demyelination was observed in pontine tissue and higher levels of caspase-3 activity were detected compared to control rats. With LINGO-1-directed siRNA-chitosan nanoparticle treatment, animals performed better than controls. Remyelination-treated group showed better motor performance than demyelination group. LINGO-1 downregulation was associated with signs of repair in histopathological sections, higher expression of pontine myelin basic protein (MBP) mRNA and protein and lower levels of caspase-3 activity indicating neuroprotection and remyelination enhancement.

The Safety of Irreversible Electroporation on Nerves Adjacent to Treated Tumors.

To evaluate the safety of irreversible electroporation (IRE) on the sciatic nerve after IRE ablation of adjacent tumor. In this study, VX2 tumors were implanted adjacent to the sciatic nerves in 26 New Zealand white rabbits. The rabbits were divided into 3 groups 10 days after implantation, with 2 treatment groups of 10 rabbits each and a control group of 6 rabbits. In 1 of the treatment groups (IRE-S group), the rabbits underwent ablation with a single IRE application, and in the other group (IRE-D group) the rabbits underwent 2 IRE applications. IRE ablation was performed under ultrasonographic guidance. The 26 rabbits were euthanized as follows: half of the animals in each group on the seventh day and the rest on the 28th day after IRE ablation. The sciatic nerves were removed for histopathologic evaluation immediately after euthanasia. Sections from selected specimens were stained with hematoxylin and eosin and Masson's trichrome method for collagen; immunohistochemistry was performed for S100 and neurofilaments (markers for Schwann cells and axons, respectively). Clinical, radiologic, laboratory, and pathologic findings were analyzed. The nerves from the IRE-S and IRE-D groups showed preserved endoneurial architecture and the presence of numerous small-caliber axons along with Schwann cell hyperplasia, consistent with axonal regeneration. The tumor lesions were completely necrosed. A fibrous scar was observed in the adjacent muscle tissue, confirming ablation at the site. Nerve damaged also showed in the control group for tumor advanced and no signs of repair; the tumor showed rapid progression. The nerves adjacent to the tumor may undergo severe damage after IRE ablation, but their function and structure can return to normal in a short time. IRE ablation may be a feasible treatment option for tumors situated adjacent to nerves.

Putative role of epithelial rests of Malassez in alleviation of traumatic occlusion

BackgroundEpithelial cell rests of Malassez (ERM) are odontogenic epithelial cells located throughout life within the periodontal matrix. It has long been thought to be a functionless remnant, though recent studies suggested their role in periodontium regeneration and homeostasis. Aim of studyThe aim of the present study was to investigate the role of ERM in alleviating the deteriorating effect of an induced primary acute traumatic occlusion in rats. Material and methodsTwenty four, 7 month old male rats were used in this study. Animals were randomly divided into two equal groups, a control and traumatic occlusion groups. Rats in the latter group had the occlusal surfaces of their right maxillary first molars unilaterally raised 1–2 mm with our innovative 7/8 nickel chrome stainless steel crowns that had free distal surfaces. Three rats, from each group, were euthanized at 1, 3, 6, and 9 weeks. Half of their right mandibular first molar-specimens were processed for light microscope (LM) and the other for transmission electron microscope (TEM). ResultsRats in the control group revealed no difference in their normal ordinary periodontal ligaments (PDL) structure, by LM, at all times. Ultrastructurally, all samples revealed similarity in having closely approximated resting ERM cells. On the other hand, after one and three weeks of traumatic occlusion, there were mild progressive PDL disorganization, cementum resorption together with phagocytic and secretory ERM cells, respectively. Interestingly, at later stages on the 6th and 9th week, signs of repair and remodeling of PDL structure were manifested along with the establishment of closely juxtaposed clusters of ERM with apoptotic and secretory characters, respectively. ConclusionERM cells appeared to have an important role within the periodontal apparatus. Their diverse ultrastructural features during periodontal deterioration and regeneration would suggest their role in alleviating the injury resulted from induced traumatic occlusion.

A new type of lordosis and vertebral body compression in Gilthead sea bream, Sparus aurata L.: aetiology, anatomy and consequences for survival

A new type of vertebral malformation is described, consisting of deformed cartilaginous neural and haemal processes and the compression and fusion of vertebral bodies. The malformation is designated as haemal vertebral compression and fusion (haemal VCF). We studied the aetiology of the malformations and described microanatomical histopathological alterations. The malformations were detected during routine quality control in one of six monitored Gilthead sea bream populations. Haemal VCF affected the posterior part of the vertebral column (haemal vertebrae). In 20% of the deformed specimens, haemal VCF was combined with lordosis. At 35 dph (days post-hatching), early anatomical signs of the haemal VCF consisted of abnormal centrum mineralization, malformed cartilaginous neural and haemal processes and developing lordotic alterations. The histological examination of the deformed individuals revealed that haemal VCF is preceded by notochord abnormalities. The frequency of deformed individuals was three times higher at 35 than at 61 dph (50.3% vs. 17.2%, n = 157 and n = 250, respectively). No signs of repair or reversion of malformations have been observed. Thus, the steep decrease in deformities in older animals suggests that haemal VCF is linked to high mortality rates. The results are discussed in respect of the possible causative factors of haemal VCF.

The manifestation of cocaine-induced midline destructive lesion in bone tissue and its identification in human skeletal remains

Cocaine-induced midline destructive lesion (CIMDL) is a condition that may arise in response to chronic insufflation (“snorting”) of cocaine. It is clinically diagnosed when the nasal septum, lateral nasal walls, and/or hard palate show signs of destruction in association with cocaine use. Although its true incidence is unknown, CIMDL is not an uncommon clinical finding amongst intranasal cocaine abusers and is likely to be encountered by forensic anthropologists and medical examiners working worldwide. Given the preponderance of drug abusers amongst the subjects of forensic casework, the ability to diagnose CIMDL in dry bone may provide crucial insight into an investigation and even help confirm an individual identification.This paper aims to make practicing forensic anthropologists aware of CIMDL. Through the analysis of existing clinical literature, patient CT scans, and histology sections, it works toward the establishment of formal diagnostic criteria for identifying CIMDL in human skeletal remains. Lytic destruction regularly involves the vomer and frequently extends to the perpendicular plate of the ethmoid, the palatal process of the maxillae or the palatine bones, and the inferior nasal conchae. The middle nasal conchae, medial walls of the maxillary sinuses, ethmoid sinuses, and cribriform plate are often damaged. Destruction may also implicate the superior nasal conchae, the orbit, and the sphenoid. Bones affected by CIMDL may contain necrotic lesions or may be absent entirely. Lesions show minimal, if any, signs of repair. The author proposes that this lack of new bone formation may be mediated by potentially elevated leptin levels in cocaine abusers and CIMDL patients and may be the key to differentiating CIMDL from other lytic processes of the midface.

Drought's legacy: multiyear hydraulic deterioration underlies widespread aspen forest die‐off and portends increased future risk

Forest mortality constitutes a major uncertainty in projections of climate impacts on terrestrial ecosystems and carbon-cycle feedbacks. Recent drought-induced, widespread forest die-offs highlight that climate change could accelerate forest mortality with its diverse and potentially severe consequences for the global carbon cycle, ecosystem services, and biodiversity. How trees die during drought over multiple years remains largely unknown and precludes mechanistic modeling and prediction of forest die-off with climate change. Here, we examine the physiological basis of a recent multiyear widespread die-off of trembling aspen (Populus tremuloides) across much of western North America. Using observations from both native trees while they are dying and a rainfall exclusion experiment on mature trees, we measure hydraulic performance over multiple seasons and years and assess pathways of accumulated hydraulic damage. We test whether accumulated hydraulic damage can predict the probability of tree survival over 2 years. We find that hydraulic damage persisted and increased in dying trees over multiple years and exhibited few signs of repair. This accumulated hydraulic deterioration is largely mediated by increased vulnerability to cavitation, a process known as cavitation fatigue. Furthermore, this hydraulic damage predicts the probability of interyear stem mortality. Contrary to the expectation that surviving trees have weathered severe drought, the hydraulic deterioration demonstrated here reveals that surviving regions of these forests are actually more vulnerable to future droughts due to accumulated xylem damage. As the most widespread tree species in North America, increasing vulnerability to drought in these forests has important ramifications for ecosystem stability, biodiversity, and ecosystem carbon balance. Our results provide a foundation for incorporating accumulated drought impacts into climate-vegetation models. Finally, our findings highlight the critical role of drought stress accumulation and repair of stress-induced damage for avoiding plant mortality, presenting a dynamic and contingent framework for drought impacts on forest ecosystems.

Subcutaneous tissue response of mice to calcium hydroxide‐based pastes combined with chlorhexidine or to chlorhexidine gel used as intracanal medication

The purpose of this study was to evaluate the response of subcutaneous connective tissue of mice to calcium hydroxide‐based pastes with chlorhexidine digluconate (CHX) or to CHX gel. Seventy‐five mice were assigned to 5 groups. Each animal received 2 polyethylene tube implants as follows: Group I (n=10 tubes) ‐ calcium hydroxide paste (Calen®), Group II (n=10) ‐ Calen mixed with 0.5% CHX (n=10), Group III (n=10) ‐ Calen mixed with 2% CHX, Group IV (n=10) −2% CHX gel, Group V (n=10) empty tube for 7, 21, and 63 days. The tissues were removed and submitted to histological processing and analysis. On days 7, group IV showed more inflammatory cells then groups I, II and III (p<0.05 ‐ ANOVA and Tukey test). On days 21, there was no difference between groups I and II (p>0.05) and between groups III and IV (p>0.05), and the number of inflammatory cells was higher in these last two groups (p<0.05). On days 63, groups I and II showed less inflammatory cells, followed by III (p<0.05) and IV (p<0.05). On days 63, groups I, II and III showed regression of the initial inflammation and signs of repair. In group IV there was no regression of inflammation suggesting a persistent residual aggression from the material, even 63 days. In conclusion, the Calen and Calen + 0.5% CHX allowed best adequate tissue response, whereas the Calen + 2% CHX showed an intermediate tissue response and 2% CHX gel showed worst tissue response. Supported by PROPe‐UNESP.

Tratamiento de una lesión endoperiodontal tipo III (combinada o verdadera): reporte de un caso

We report a case of a type III periodontal-endodontic lesion (combined or true) in a 41-year-old female patient without systemic history. The patient was transferred from the Specialization Course in Periodontology at the Graduate School of the University of Chile due to a periapical lesion in the tooth 3.6. The prognosis for this type of lesion is uncertain, since it is necessary to perform endodontic and periodontal treatment, and the result depends more on the periodontal treatment. The piece was treated endodontically leaving intracanal medication based on 2% Chlorhexidine gel for 7 days. Once the tooth obturated, we gave the patient an appointment 3 months later for a control radiography. Currently, the tooth is completely asymptomatic, without mobility and with signs of repair.

Orthodontic tooth movement into edentulous ridge areas--a case series

The aim of this case series was to analyse dimensional alterations of the alveolar ridge and tooth-supporting structures, as well as root resorption, following orthodontic tooth movement into edentulous areas with reduced ridge dimensions. The study involved six subjects (30-70 years) with 10 edentulous jaw areas in the premolar regions. Clinical and radiographic examinations and 3D measurements on scanned study casts were performed at baseline, at retention, and after 1 year of (i) the edentulous area into which the tooth was moved and (ii) the established edentulous area from which the tooth was moved. The orthodontic tooth movement into an edentulous area resulted in most individuals in only minor dimensional alterations of the periodontal tissues. With regard to the width of the alveolar process, the results indicated a decreased width in the newly established edentulous area, whereas in the area into which the tooth had been moved, the width increased. In all cases, the moved tooth showed lateral root resorption on its pressure side at the level of the bone crest at time of retention, but signs of repair were noticed at the 1-year follow-up. Within the limitations of the study, it can be concluded that orthodontic tooth movement results in dimensional alterations of the edentulous ridge and that lateral root resorption is an inevitable side-effect.

Low Level Primary Blast Injury in Rodent Brain

The incidence of blast attacks and resulting traumatic brain injuries has been on the rise in recent years. Primary blast is one of the mechanisms in which the blast wave can cause injury to the brain. The aim of this study was to investigate the effects of a single sub-lethal blast over pressure (BOP) exposure of either 48.9 kPa (7.1 psi) or 77.3 kPa (11.3 psi) to rodents in an open-field setting. Brain tissue from these rats was harvested for microarray and histopathological analyses. Gross histopathology of the brains showed that cortical neurons were “darkened” and shrunken with narrowed vasculature in the cerebral cortex day 1 after blast with signs of recovery at day 4 and day 7 after blast. TUNEL-positive cells were predominant in the white matter of the brain at day 1 after blast and double-labeling of brain tissue showed that these DNA-damaged cells were both oligodendrocytes and astrocytes but were mainly not apoptotic due to the low caspase-3 immunopositivity. There was also an increase in amyloid precursor protein immunoreactive cells in the white matter which suggests acute axonal damage. In contrast, Iba-1 staining for macrophages or microglia was not different from control post-blast. Blast exposure altered the expression of over 5786 genes in the brain which occurred mostly at day 1 and day 4 post-blast. These genes were narrowed down to 10 overlapping genes after time-course evaluation and functional analyses. These genes pointed toward signs of repair at day 4 and day 7 post-blast. Our findings suggest that the BOP levels in the study resulted in mild cellular injury to the brain as evidenced by acute neuronal, cerebrovascular, and white matter perturbations that showed signs of resolution. It is unclear whether these perturbations exist at a milder level or normalize completely and will need more investigation. Specific changes in gene expression may be further evaluated to understand the mechanism of blast-induced neurotrauma.

Morbid anatomy of ‘erosive osteoarthritis’ of the interphalangeal finger joints: an optimised scoring system to monitor disease progression in affected joints

ObjectivesTo develop and validate a quantitative radiographic scoring system, the Ghent University Scoring System (GUSS), with better ability to detect progression over a shorter period of time in erosive osteoarthritis...

Interstitial telomeric sequences (ITSs) are not located at the exact evolutionary breakpoints in primates

Although their function has not yet been clearly elucidated, interstitial telomeric sequences (ITSs) have been cytogenetically associated with chromosomal reorganizations, fragile sites, and recombination hotspots. In this paper, we show that ITSs are not located at the exact evolutionary breakpoints of the inversions between human and chimpanzee and between human and rhesus macaque chromosomes. We proved that ITSs are not signs of repair in the breakpoints of the chromosome reorganizations analyzed. We found ITSs in the region (0.7–2.7 Mb) flanking one of the two breakpoints in all the inversions assessed. The presence of ITSs in those locations is not by chance. They are short (up to 7.83 repeats) and almost perfect (82.5–97.1% matches). The ITSs are conserved in the species compared, showing that they were present before the reorganizations occurred.

Cellular and extracellular factors in early root resorption repair in the rat

The aim of this study was to investigate the role of extracellular matrix components, such as collagen type I, fibronectin, and osteopontin (OPN) during cementum repair following experimentally induced tooth movement, and to characterize the cells taking part in the regenerative process. The upper right first molars were moved mesially in 21 three-month-old male Wistar rats using a coil spring with a force of 0.5 N. After 9 days, the appliance was removed and the animals were killed in groups of three immediately after withdrawal of the force and 5, 7, 10, 12, 14, and 17 days later. Three rats served as non-experimental control animals. The maxillae were prepared and processed for histological analysis. Together with the disappearance of the multinucleated odontoclasts from the resorption lacunae, signs of repair were visible 5 days after the release of the orthodontic force. The first signs of cementum repair were seen on day 10. The newly produced cementum was of the acellular extrinsic fibre type (AEFC) and reattachment was achieved with the principal periodontal ligament (PDL) fibres orientated almost perpendicular to the root surface. The initial interface formed between the old and new cementum, as well as the new AEFC, was characterized by a strong immunoreaction with OPN and collagen I antibody, but only a weak immunoreaction with the fibronectin antibody. Only a small number of mononuclear cells, which were involved in the repair process, showed a positive immunoreaction with the osteoblastic lineage markers runt-related transcription factor 2 and osteocalcin. These same cells stained sparsely with muscle segment homeobox homologue 2, but not with the E11 antibody. Thus, most of the cells associated with this reparative activity on the surface of the lacunae were differentiated PDL cells of the fibroblastic phenotype. Cells with a defined osteoblastic phenotype seemed to be of minor importance in this repair process.

Lower Tidal Volumes and Positive End-expiratory Pressure Prevents Alveolar Coagulation in Patients without Lung Injury

University of Louisville, Louisville, Kentucky. ozan.akca@louisville.eduI read with interest the excellent article by Choi et al. 1about the preventive role of mechanical ventilation, with lower tidal volumes plus positive end-expiratory pressure (PEEP), on alveolar coagulation. They demonstrated that mechanical ventilation with lower tidal volumes and PEEP (10 cm H2O) decreases the procoagulant activity in the lungs of even otherwise healthy surgical patients. The observed procoagulant activity change was explained by mechanical ventilation with high tidal volume and no PEEP. In previous studies, the same researchers and others showed that there were similar pulmonary hemostasis disturbances in patients with adult respiratory distress syndrome and pneumonia. Although much is unknown about the topic, the authors gave a detailed discussion as to whether this procoagulant activity is a possible sign of repair or a further trigger of proinflammatory process in the lung.If we exclude this important work by Choi et al. , the recent literature provides conflicting evidence on the role of high-tidal volume with no PEEP in causing ventilator-associated lung injury in healthy human lungs.2–4Possibly because of the short amount of time that mechanical ventilation is provided during general anesthesia, it was hard to see any clinical effects of potential lung stretch in relatively healthy human lungs. Another explanation would be that high-tidal-volume ventilation alone is not a sufficient trigger to cause lung injury in healthy human lungs. Two recent articles from Wrigge et al. 4,5support the latter explanation. Accepting this, one can hypothesize that mechanical ventilation with high tidal volumes without PEEP does not initiate any tissue injury that can be monitored by proinflammatory cytokine response.However, when we take the article by Choi et al. into account and further consider the bidirectional relation between coagulation and inflammation in pathogenesis of vascular disease as well summarized previously by Levi et al. ,6we realize that there are different questions to be asked and various hypotheses to be made to fully understand the mechanism of ventilator-associated lung injury in previously healthy subjects. For example, what might be the absolute first trigger to initiate stretch injury in the lungs? As in the vascular pathophysiology, is it the direct stretch of mononuclear cells (in this case alveolar macrophages) that triggers the proinflammatory or procoagulant pathways? Is it a set of proinflammatory cytokines originating from the alveolar macrophages (or even epithelial cells) triggering the procoagulant process in the lungs? Can such processes be triggered by lung cellular stretch through the activation of integrin–mitogen-activated protein kinase–interleukin-8 pathway, which would lead to further chemokine responses?7,8Or do any of the toll-like receptors play a triggering role in initiating transcriptional processes through nuclear factor κB to deliver proinflammatory pathways including tumor necrosis factor α or interleukin 1β? Can it be that high-tidal-volume, no-PEEP ventilation cancels the alveolar integrity and stability of alveolar macrophages maintained by transforming growth factor β?9The sequence of triggers would bring the real mechanisms behind the ventilator-associated lung injury and associated lung injury. Therefore, it is extremely important to understand the sequence of triggers and potential pathways. At this point, if Choi et al. performed any other tests in the bronchoalveolar lavage samples, such as proinflammatory cytokines, chemokines, or any transcriptional pathway agents, simultaneously with their procoagulant tests, it would be valuable to share such data for further development of new hypotheses to test the bidirectional relation between coagulation and inflammation.University of Louisville, Louisville, Kentucky. ozan.akca@louisville.eduThe author thanks Nancy Alsip, Ph.D. (University of Louisville, Louisville, Kentucky), for editorial assistance.

Clinical and Histological Experimental Investigation of Temporomandibular Joint Traumatic Arthritis

Objective: To investigate the symptoms and pathology related to classification of temporomandibular joint traumatic arthritis (TMJTA) and the use of classification of various forms. Methods: The clinical and imaging data of 41 patients with TMJTA caused by joint blunt trauma, 32 patients with chronic TMJTA caused by condylar fractures and 6 patients with a long time opening limitation after condylar fractures were included in the present study. In addition, the pathology of an experimental rabbit model of traumatic arthritis model of rabbit was examinedand investigated pathologically. Results: Joint movement restriction was found in most patients with TMJTA. The iImaging results findingsrevealed were bony degenerative changes, disc displacement, and joint adhesion in the patients with TMJTA caused by blunt trauma and condylar deformity in the patients with TMJTA caused by condylar fractures. In the experimental rabbits, hemorrhages, and condylar and disc damage could be seen in the early stage and signs of repair were seenrepairing action in the later stage of acute trauma. Conclusion: The causes of TMJTA canould be classified into two types: which was caused by joint blunt trauma and condylar fractures. The time boundary of acute and chronic TMJTA caused by blunt trauma and TMJTA caused by condyle fractures was suggested as one and six months respectively. The time boundary of acute and chronic TMJTA caused by blunt trauma and TMJTA caused by condylar fractures was suggested as one month and half a year respectively.

Spatial tuning curves along the chick basilar papilla in normal and sound-exposed ears.

Intense sound exposure destroys chick short hair cells and damages the tectorial membrane. Within a few days postexposure, signs of repair appear resulting in nearly complete structural recovery of the inner ear. Tectorial membrane repair, however, is incomplete, leaving a permanent defect on the sensory surface. The consequences of this defect on cochlear function, and particularly frequency analysis, are unclear. The present study organizes the sound-induced discharge activity of cochlear nerve units to describe the distribution of neural activity along the tonotopic axis of the basilar papilla. The distribution of this activity is compared in 12-day postexposed and age-matched control groups. Spontaneous activity, tuning curves, and rate-intensity functions were measured in each unit. Discharge activity at 60 frequency and intensity combinations was identified in the tuning curves of hundreds of units. Activity at each of these criterion frequency/intensity combinations was plotted against the unit's characteristic frequency to construct spatial tuning curves (STCs). The STCs depict tone-driven cochlear nerve activity along the length of the papilla. Tuning sharpness, low- and high- frequency slopes, and the maximum response were quantified for each STC. The sharpness of tuning increased with increasing criterion frequency. However, within a frequency, increasing sound intensity yielded more broadly tuned STCs. Also, the high-frequency slope was consistently steeper than the low-frequency slope. The STCs of exposed ears exhibited slightly less frequency selectivity than control ears across all frequencies and larger maximum responses for STCs with criterion frequencies spanning the tectorial membrane defect. When rate-intensity types were segregated, differences were observed in the STCs between saturating and sloping-up units. We propose that STC shape may be determined by global mechanical events, as well as localized tuning and nonlinear processes associated with individual hair cells. The results indicated that 12 days after intense sound exposure, global and local contributions to spatially distributed neural activity are restored.

Effect of 50 Hz, 0.2 mT magnetic fields on RBC properties and heart functions of albino rats.

In this work the effect of sinusoidal 50 Hz, 0.2 mT magnetic fields on the red blood cells (RBCs) and heart functions of Albino rats were investigated. Twenty-four male Albino rats were equally divided into four groups, A, B, C, and D. Animals from groups B were continuously exposed to the magnetic field for 15 days; and groups C and D, for 30 days. Group A was used as control. Animals from group D were kept after exposure to the magnetic field for a period of 45 days for delayed effect studies. The osmotic fragility and shape of RBCs' membrane and hemoglobin (Hb) structure tests were carried out for all groups. The dielectric relaxation of Hb molecules was measured in the frequency range of 0.1-10 MHz and the dielectric increment (Deltaepsilon), relaxation time (tau), molecular radius (r), and Cole-Cole parameter (alpha) were calculated for all groups. The ECG was measured for all animals before and after exposure to the magnetic field. The results indicated that exposure of the animals to 50 Hz, 0.2 mT magnetic fields resulted in the decrease of RBCs membrane elasticity and permeability and changes in the molecular structure of Hb. The ECG of the exposed animals was considerably altered. The data also indicated that there was no sign of repair in the newly generated RBCs structure and the ECG after removing the animals from the magnetic field, which indicates that the blood generating system was severely injured. The injuries in the heart of the animals were attributed to the loss of some physiological functions of the RBCs as a result of exposures of the rats to the magnetic field.

Root resorption and signs of repair in Papillon-Lefèvre syndrome. A case study

The aim of this investigation was to describe some tooth-related histological features of prepubertal periodontitis. Teeth extracted during treatment of two Papillon-Lefèvre syndrome patients were processed by means of the sawing and grinding technique. Light microscopy examination revealed little or no cementum in the coronal parts of the roots. Resorptions of various depths (0.02 to 1.5 mm) and to various extents (affecting up to 1/3 of the root surface) were observed in the 5 investigated teeth. Some resorptive defects on 1 of the examined incisors showed signs of spontaneous repair. Extrinsic fibers were inserted into the new cellular intrinsic fiber cementum which had formed directly on the bottom of the defect. Intact acellular extrinsic fiber cementum was found where fibers were still attached. Here, the characteristic of pristine cementum, a hyaline layer of peripheral dentin, could be identified. If resorption was not present, the cementum did not show any signs of hypoplasia. Thus, histological features of prepubertal periodontitis in the current material were (i) areas of extensive resorption, (ii) signs of spontaneous repair, and (iii) healthy cementum.