[Autopneumonectomie. A Forgotten Disease]. / Autopneumonektomie. Ein vergessenes Krankheitsbild.

HISTORY: An 80-year old female was referred to our hospital with left internal carotid artery stenosis and a childhood history of hemoptysis. INVESTIGATIONS AND DIAGNOSIS: The ECG showed 2nd degree Mobitz atrio-ventricular block. The chest x-ray and computerized tomography identified a shift of the mediastinum and the heart to the left. The left lung was completely destroyed whilst the right lung was enlarged and crossed the midline. Pulmonary function tests revealed a moderate restrictive ventilation disorder. The diagnosis of autopneumonectomy was based on patient history together with radiological findings. TREATMENT AND COURSE: A pacemaker was implanted with two stimulation electrodes via a left cephalic venous cutdown. A carotid endarterectomy was also performed without any complication. CONCLUSION: After autopneumonectomy, postpneumonectomy like syndrome may occur in very rare cases, whereupon operative treatment is mandatory. Any respiratory infections should be treated with antibiotics. Pacemaker electrode placement via the subclavian vein is contraindicated due to the risk of a catastrophic pneumothorax.

Multiple left ventricular inferoseptal clefts. Multimodality imaging appearance and differential diagnosis.

BACKGROUND: Left ventricular inferoseptal clefts are a localized variant of myocardial structure, easily overlooked but potentially raising concern when identified through imaging. CASE STUDY: Here we illustrate and describe inferoseptal clefts by means of multimodality imaging and consider them in relation to possible differential diagnoses. A 49-year-old male patient was investigated for chest pain and found to have multiple inferoseptal clefts. The pain subsequently resolved and was thought to have been pleuritic. There was no evidence or family history of hypertrophic cardiomyopathy. The diagnosis of clefts was arrived at after consultation with several cardiac imaging specialists and the few available relevant published reports. Echocardiography, cardiovascular magnetic resonance, invasive ventriculography and computed tomography each showed the clefts in relation to surrounding compact and contractile myocardium of the inferoseptal region, which occluded the clefts in systole. In terms of location, orientation and systolic occlusion the inferoseptal clefts resembled the isolated clefts reported in healthy volunteers, and have features in common with crypts reported in carriers of a genetic mutation associated with hypertrophic cardiomyopathy (HCM). The incidence and implications of multiple inferoseptal clefts have yet to be determined. CONCLUSION: Multimodality imaging permits clear depiction of left ventricular inferoseptal clefts, which should be distinguished from different entities such as left ventricular noncompaction cardiomyopathy (LVNC), cardiac diverticula and cardiac aneurysms. Inferoseptal clefts have yet to be widely recognized as a distinct variant of regional left ventricular structure.

Metabolism of alveolar cells: histochemical evidence and relation to pulmonary surfactant.

Large alveolar cells of normal dog lung are rich in enzymes concerned with oxidative and synthetic pathways. In three experimental situations where ability of the lung to produce surfactant was impaired, the enzyme-rich cells were lacking or absent. Findings support the concept that these cells are sites of active metabolism, possibly including production of surfactant.

Oestrogen increases nociception through ERK activation in the trigeminal ganglion: evidence for a peripheral mechanism of allodynia.

The mitogen-activated protein kinase, extracellular signal-regulated kinase (ERK), is activated in experimental models of chronic pain, and is also activated by oestrogen. We used an established model of inflammatory trigeminal pain, injection of Complete Freund's Adjuvant (CFA) into the masseter muscle, to determine whether ERK activation may play a role in hormone-related trigeminal pain disorders. We measured withdrawal responses to stimulation of the masseter (V3, primary allodynia) and whisker pad (V2, secondary allodynia) using graded monofilaments. Oestrogen treatment in the presence of inflammation increased withdrawal response to stimulation of both masseter and whisker pad compared with inflammation alone, indicating an additive effect of inflammation and oestrogen on both primary and secondary allodynia. We examined ERK activation in trigeminal ganglia from each treatment group using western blot and immunohistochemistry. Both masseter inflammation and oestrogen treatment increased ERK activation, and combined treatment had an additive effect. Both masseter inflammation and oestrogen increased the percentage of pERK immunoreactive neurons in divisions 1 and 2 (V1/2), and combined treatment increased pERK immunoreactivity in V1/2 compared with inflammation alone. We stereotactically administered ERK antagonist U0126, or inactive control U0124, to the trigeminal ganglion of CFA+E2-treated rats. U0126 decreased withdrawal responses to mechanical stimulation of the whisker pad compared with U0124-treated rats. Because the secondary allodynia in V2 after inflammation in V3 was reduced by antagonizing ERK activation in the periphery, these data suggest a peripheral component to secondary allodynia mediated through ERK activation.

On the selection of endogenous and exogenous signals.

Alerting is one of the three components of attention which involves the eliciting and maintenance of arousal. A seminal study by Posner et al. (Posner MI, Klein R, Summers J, Buggie S. 1973 Mem. Cognit. 1, 2-12 (doi:10.3758/BF03198062)) focused on how changing the interval between an alerting signal and a target would impact the speed and accuracy of responding. Participants indicated whether targets were presented on the left or right side of the fixation point. Auditory warning signals were played at various intervals prior to the target to alert participants and prepare them to make a response. Reaction times revealed a robust, U-shaped, preparation function. Importantly, a clear speed-accuracy trade-off (SAT) was observed. In the current experiment, we replicated the methodological components of this seminal study while implementing a novel auditory warning signal (Lawrence MA, Klein RM. 2013 J. Exp. Psychol. General 142, 560 (doi:10.1037/a0029023)) that was either purely endogenous (change in quality without a change in intensity; analogous to isoluminant colour change in vision) or a combination of endogenous and exogenous (change in both quality and intensity). We expected to replicate the U-shaped preparation function and SAT observed by Posner and colleagues. Based on Lawrence and Klein's findings we also expected the SAT to be more robust with the intense signal in comparison to the isointense signal.

The independence of endogenous and exogenous temporal attention.

Temporal attention is the focusing of perceptual resources at a particular point in time. Valid temporal cue information has the capability to improve performance by reducing reaction times, while invalid information has the possibility of impairing performance. The performance difference between valid and invalid conditions is called a temporal cueing effect (TCE). We explored how different alerting mechanisms interact with a participant's ability to utilize temporal information cues, using the Kingstone (The Quarterly Journal of Experimental Psychology, 44(1), 69-104, 1992) temporal cueing paradigm. Extracting the alerting procedure from Lawrence and Klein (Journal of Experimental Psychology: General, 142(2), 560-572, 2013), one of two different temporally contingent warning signals were presented to participants during a trial. The "hi-intensity" warning signal increases intensity and elicits both exogenous and endogenous alerting mechanisms. The "no-intensity" warning signal is isointense relative to baseline and elicits only endogenous alerting mechanisms. Two experiments conducted previously using a discrimination task showed interference between the signal intensity and task difficulty, where the "no-intensity" signal failed to elicit TCEs. In the present study, we implemented a detection task, reducing the mental effort required for a response. The results showed equal TCEs in both signal conditions. We argue for independence of these alerting mechanisms, by way of Sternberg's (Acta Psychologica, 30, 276-315, 1969) additive factor method. Arguments contrasting what mechanism is being impacted by this paradigm are further outlined.

Kinetics of mast cell, fibroblast, and epidermal cell proliferation during acute graft-versus-host disease in the neonatal rat.

Acute graft-versus-host disease (GVHD) was induced in newborn Brown-Norway (BN) and DA rats by i.v. injection of 3 X 10(7) Lewis (L) lymph node cells. Control BN and DA rats received syngeneic cells. Rats were injected i.v. with [methyl-3H]thymidine for 1 h before being killed at 1, 2, 4, 5, 6, 8, 10, 11, 12, 13, and 14 days after the cellular inoculum. A piece of ventral abdominal skin was removed. Autoradiography was used to determine cell proliferative activity (labeling index, LI) in mast cells and fibroblasts of the dermis and basal cells of the epidermis. In addition, the number of mast cells per high-power field was determined for all 4 groups of rats: control DA, GVHD-DA, control BN, and GVHD-BN. Only GVHD-BN rats demonstrated extensive dermatitis. The LI of mast cells, fibroblasts, and basal cells decreased in control rats with increasing age. Although there were differences between DA and BN rats, there was a general pattern of increased proliferation of mast cells at early time points of GVHD followed by a decrease to or below control levels. The number of mast cells per high-power field also increased at early time intervals in both the DA and BN GVHD rats, but decreased significantly at later time points. These data confirm previous studies on chronic GVHD which demonstrated a decrease in the number of mast cells in the skin. Fibroblast LI was decreased at day 1 in both DA and BN GVHD rats. In GVHD-DA, fibroblast LI remained depressed while GVHD-BN demonstrated a second peak in LI at day 10 before declining below control levels. The most prominent basal cell response occurred in GVHD-BN between days 6-14 and is probably indicative of an attempted reparative response associated with GVHD dermatitis in this species. These data demonstrate that the activation of mast cells (proliferation and subsequent degranulation) correlates temporally with cell kinetic alterations occurring in the dermis and epidermis during acute GVHD.

A review of the evidence for a disengage deficit following parietal lobe damage.

We review the literature on response times to ipsilesional and contralesional targets following spatial precues in patients with damage involving the left- and right-parietal lobes with the aim of appraising the 'disengage deficit' reported initially by Posner and colleagues (Posner MI, Cohen A, Rafal RD. Neural systems control of spatial orienting. Proceedings of the Royal Society of London, B 1982;298:187-98). The data of individual subjects from a sub-sample of studies were submitted to analyses of variance, and data from all studies meeting our selection criteria were submitted to meta-analytic procedures (Hunter JE, Schmidt FL. Methods of meta-analysis: correcting error and bias in research. Newberg Park: Sagge Publications, 1990). Findings from both types of analysis conducted on data from patients with right-hemisphere lesions indicate that: (1) the disengage deficit phenomenon is robust following peripheral cues, but not following central cues; (2) the disengage deficit is large at shorter cue-target stimulus onset asynchronies (SOAs), and decreases as SOA increases; (3) the disengage deficit is larger in patients with a diagnosis of hemispatial neglect; and (4) although the magnitude of the disengage deficit appears to increase with increases in lesion size, multilobar vs unilobar involvement did not significantly alter the pattern of the disengage deficit. We also show that responses to validly cued targets in the contralesional hemispace were significantly slower than for validly cued targets in ipsilesional hemispace. Similar, but usually smaller, effects were observed in patients with homologous left-hemisphere damage. The implications of these results for current models of the role of the parietal lobes in attentional orienting are discussed.

Estrogen and tamoxifen interplay with T(3) in male rats: pharmacologically distinct classes of estrogen responses affecting growth, bone, and lipid metabolism, and their relation to serum GH and IGF-I.

Estrogen (E) and T(3) regulate gene expression by receptor mechanisms that may enable hormonal interplay affecting growth and metabolism. Prior studies of E and tamoxifen (TM) interplay with T(3) in female rats identified a subset of E responses that required T(3) for expression and exhibited large agonist responses to TM. In contrast, TM acted more like an antagonist in most T(3)-independent E responses. This study used male rats to further explore the role of T(3) in E effects on growth and metabolism, and the relation of such effects to changes in serum GH and IGF-I. Orchidectomized, hypothyroid rats were treated 6 wk with vehicle, E2 benzoate (E2B), or TM with or without T(3). The following parameters were measured: body weight change; tibia length and bone mineral density; heart and kidney weight; food intake and body temperature; serum levels of glucose, cholesterol, triglycerides, GH, and IGF-I; seminal vesicle weight; and anterior pituitary levels of GH, PRL, glandular kallikrein, and total protein. Interplay with T(3) contributed to multiple E effects on growth and metabolism, and some E responses involved both T(3)-dependent and T(3)-independent components. Both E2B and TM increased serum GH, but the increases were poorly coupled to IGF-I. Correlation/regression analysis of individual rat data sets suggested distinct roles for GH and IGF-I in specific E effects. E2B and TM effects on somatic growth exhibited positive correlations with IGF-I and negative correlations with GH; effects on bone mineral density and triglycerides exhibited positive correlations with GH and negative correlations with IGF-I. Three pharmacologically distinct classes of in vivo E responses were identified in this study, and TM displayed a profile of biological activity that may be useful for men undergoing androgen-deprivation therapy.

The effects of nicotine on spatial and non-spatial expectancies in a covert orienting task.

The present study examined how nicotine influences shifts of visuo spatial attention in casual smokers at each of three delays after smoking one cigarette: immediately, 1 h and 24 h. Informative peripheral cues were used to exogenously orient attention to the location where an increase or decrease in the size of a peripheral object was most likely to occur. One size change was more likely to occur than the other and the task was choice (expansion/contraction) reaction time. The performance decrement obtained when the target appeared at an uncued location was smallest in sessions run immediately after smoking (when nicotine levels were highest), suggesting that nicotine may increase the ease with which attention can be disengaged from a cued location. This finding confirms previous research which suggests a specific role for the basal forebrain cholinergic system in visual orienting. In contrast, nicotine was not found to affect non-spatial expectancies based on stimulus-response (expansion/contraction) probability. These findings, together with recent converging evidence, strongly support the proposition that different attentional operations are mediated by different neural subsystems.

Histomorphological studies of the distal internal thoracic artery which support its use for coronary artery bypass grafting.

The use of the internal thoracic artery (ITA) for myocardial revascularization in coronary artery disease increased because of its relative immunity to atherosclerotic obstruction. This study investigated the distal part of the vessel, the region of anastomosis by means of histology to focus the visualization of this region of interest. The histological examination of arterial segments showed minor intimal thickening in 48 out of 100 patients. Twelve patients demonstrated a severe intimal thickening, the residual patients were without any changes. In 52% the elastic type dominated in the distal part. Hybrid and muscular patterns were found in 22 and 26%, respectively. The media could be classified into three different types: muscular, hybrid and elastic type. There was no correlation concerning the different histological type and the incidence of intimal thickening. No evidence whatsoever of atherosclerotic lesion was encountered in any of the investigated vessels. There is no limitation in the use of the distal part of the ITA for coronary artery revascularization.

Diagnostic procedures for Paget's disease. Radiologic, pathologic, and laboratory testing.

Paget's disease is a relatively common skeletal disorder that affects older individuals. Although its causes are unknown, it is characterized by abnormal remodeling and a high rate of bone turnover that determines its pathologic, radiologic, and biochemical findings. The findings in the three phases of Paget's disease are described.

Atrial natriuretic peptide-like immunoreactivity in neurons and astrocytes of human cerebellum and inferior olivary complex.

Atrial natriuretic peptide (ANP) has previously been localized in areas of mammalian brain associated with olfaction, cardiovascular function, and fluid/electrolyte homeostasis. Despite the presence of several types of natriuretic peptide receptors in mammalian cerebellum, neither intrinsic nor extrinsic sources of the natriuretic peptides have been described. In this report we describe the immunohistochemical localization of both intrinsic and extrinsic sources for ANP in human cerebellum. ANP-like immunoreactivity (ANP-LIR) was observed in climbing fibers in the cerebellar molecular layer that probably originated from isolated immunopositive neurons of the inferior olivary complex. Intrinsic sources of ANP-LIR included small subpopulations of protoplasmic and fibrous astrocytes and Bergmann glia, as well as Golgi and Lugaro neurons of the granule cell layer. These results suggest that, in addition to its presumptive roles in local vasoregulation, ANP may serve as a modulator of the activity of Purkinje neurons.

Sacrococcygeal dysgenesis association.

In the malformation analysis of 445 patients ascertained only for a sacrococcygeal malformation, a new phenotype, the sacrococcygeal dysgenesis association (SDA), was delineated in 34%. In addition, sirenomelia patients were found in 12%, the VATER association in 27%, and 27% could not be classified. Heterogeneity in the patients with sacrococcygeal malformations was identified by the differences found in their associated malformations. SDA patients have a relatively small average number (3.3) of anomalies per patient as compared with 9.3 in sirenomelia and 6.2 in VATER patients. SDA abnormalities occurred to a significant degree only in 6 of 20 designated malformation categories (vertebral, rib, pelvic, lower limb, central nervous system [CNS], renal) in contrast to 17 in VATER and 18 in sirenomelia patients. The SDA vertebral malformation pattern also differed from that of VATER/sirenomelia patients as did the high sacrococcygeal agenesis:dysgenesis ratio and low thoracolumbar vertebrae and/or rib hypersegmentations. Most significantly, SDA patients had a large number of CNS anomalies and CNS-related dysfunctions of the urinary and distal intestinal tracts but no anatomic urinary or intestinal tract malformations. This contrasted sharply with the markedly increased occurrences of anatomic abnormalities in these body regions of the sirenomelia and VATER patients. Demographic data such as patient survival, twinning and, particularly, the high (28%) incidence of maternal diabetes in the SDA further support its differentiation from VATER/sirenomelia patients.

Deletion of 16q with prolonged survival and unusual radiographic manifestations.

Deletion of 16q is characterized by mental retardation, microcephaly, a characteristic combination of minor facial anomalies, and broad halluces. Various break points have been described. This patient's phenotype is typical of this syndrome, but in addition, unusual radiographic findings were present. This chromosome abnormality is compatible with survival into adulthood. Expression of this phenotype does not appear to be correlated with specific break points.

Multisensory prior entry.

Despite 2 centuries of research, the question of whether attending to a sensory modality speeds the perception of stimuli in that modality has yet to be resolved. The authors highlight weaknesses inherent in this previous research and report the results of 4 experiments in which a novel methodology was used to investigate the effects on temporal order judgments (TOJs) of attending to a particular sensory modality or spatial location. Participants were presented with pairs of visual and tactile stimuli from the left and/or right at varying stimulus onset asynchronies and were required to make unspeeded TOJs regarding which stimulus appeared first. The results provide the strongest evidence to date for the existence of multisensory prior entry and support previous claims for attentional biases toward the visual modality and toward the right side of space. These findings have important implications for studies in many areas of human and animal cognition.

Early and specific expression of monocyte chemoattractant protein-1 in the thalamus induced by cortical injury.

For many years it has been known that retrograde degeneration of thalamic neurons occurs following damage to the cerebral cortex, however, the molecular mechanisms which control this process are unknown. Recent studies have demonstrated microglial activation in thalamic nuclei well before the onset of retrograde neuronal cell death. Activated monocytes and microglia synthesize factors detrimental to neuronal survival as well as phagocytose damaged and dying neurons. Our previous studies demonstrated that monocyte chemoattractant protein-1 (MCP-1), a beta chemokine which attracts cells of monocytic origin to sites of injury, is rapidly expressed in the brain following visual cortical lesions. The present study examined the expression of MCP-1 messenger RNA and protein in the thalamus following a visual cortical lesion. Aspiration lesions of visual cortex were made in adult mice. At specific times after lesion, brains were harvested and dissected into specific regions. MCP-1 message as detected using northern analysis was absent in uninjured brain, but was elevated in the ipsilateral thalamus as rapidly as 1 h following the lesion. In situ hybridization localized MCP-1 message to subpial glial cells of the lateral geniculate nucleus (LGN) of the ipsilateral thalamus after injury. ELISA showed that MCP-1 protein levels were significantly elevated in the ipsilateral thalamus at 6 h, peaked at 12 h, and remained above baseline levels for at least 1 week post lesion. In addition, anti-GFAP staining demonstrated activated astrocytes localized to the ipsilateral LGN at 24 and 72 h after injury. The early expression and regional localization of MCP-1 mRNA and protein strongly suggest that MCP-1 is a critical molecule in the regulation of thalamic retrograde neuronal degeneration.

Increased chemokine gene expression during aging in the murine brain.

Normal aging results in changes in the brain that contribute to the decline of various functions, including learning and memory. Mechanisms causing this decline have not been clearly established. Activation of microglia is associated with the normal aging process in rodents and primates. Microglial activation is regulated by chemokine gene expression, and activated microglia produce substances that can be detrimental to surrounding cells. In this study we determined whether changes in chemokine expression occur during normal aging in the mouse brain. RNA samples taken from the cortex, midbrain, hippocampus, and cerebellum of 4-, 10-, 21- and 30-month-old C57BL6/DBA2 mice were analyzed for changes in gene expression. RNase protection assays were used to examine a panel of chemokines. Increased expression of macrophage inflammatory protein (MIP)-1alpha, MIP-1beta, and RANTES occurred in all four regions of the brains in the oldest mice. These increases were first detectable at 21 months of age. Increases in MIP-1alpha, MIP-1beta, and RANTES protein levels were also detected in the brains of old mice, as measured by ELISA. Increased microglial activation in the brains of 30-month-old mice, as detected by immunohistochemistry using F4/80 antibodies, correlated with increases in chemokine expression. The observed increases in chemokine gene expression that occur in conjunction with increased microglial activation suggest that chemokines may contribute to the decreased brain function that occurs during normal aging.

Selective chemokine mRNA expression following brain injury.

Injury in non-neuronal tissues stimulates chemokine expression leading to recruitment of inflammatory cells responsible for orchestration of repair processes. The signals involved in directing repair of damage to the brain are less well understood. We hypothesized that following brain injury, chemokines are expressed and regulate the rate and pattern of inflammatory cell accumulation. The two chemokine subfamilies are alpha(alpha)-chemokines, which primarily function as neutrophil chemoattractants, and the beta(beta)-chemokines, which function primarily as monocyte chemoattractants. We assessed alpha and beta chemokine mRNA expression patterns and leukocyte accumulation following a cerebral cortical lesion. Cortical lesions were produced with and without addition of endotoxin, Escherichia coli lipopolysaccharide (LPS), which stimulates cytokine expression. We studied the expression of the beta-chemokines: monocyte chemoattractant protein (gene product JE; MCP-1/JE), macrophage inflammatory protein-1 alpha and beta (MIP-1alpha and MIP-1beta), and the regulated upon activation normal T expressed and secreted chemokine (RANTES) as well as the alpha-chemokines: interferon-gamma-inducible protein (IP-10) and N51/KC (KC; a murine homologue of MIP-2). Changes in gene expression were analyzed by Northern analysis at different time points following injury. Leukocyte and macrophage densities were analyzed by immunohistochemistry at the same time intervals. All chemokines were elevated following cortical injury/endotoxin. MCP-1 and MIP-1alpha were elevated at 2 h and peaked 6 h, MIP-1beta peaked at 6 h, but declined more rapidly than MCP-1 or MIP-1alpha, and IP-10 peaked at 6 h and showed the most rapid decline. KC was elevated at 1 h, and peaked at 6 h following LPS. RANTES was elevated at 1 h and achieved a plateau level between 6 and 18 h, then declined. In contrast, sterile injuries produced in the absence of endotoxin only induced the mRNA of the beta-chemokine MCP-1, and its expression was delayed compared to the cortical injury/endotoxin group. The presence of chemokine message as early as 1 h indicates that expression of this class of molecules is an early response in the repair process following traumatic brain injury. Macrophage/microglia accumulation occurred more rapidly, activated microglia further from the lesion border, and more cells accumulated in cortical injury/endotoxin than in cortical lesions produced under sterile conditions. Thus, there was a positive correlation between beta-chemokine expression and the number of beta-chemokine responsive cells (i.e. microglia) accumulating in injury sites. This is the first comprehensive study using a panel of chemokine probes and specific marcophage/microglial markers to study in vivo activation of the brain following injury. Our data show that the brain is capable of expression of multiple chemokine genes upon appropriate stimulation (e.g. LPS-treatment). The gradient of microglial activation is consistent with physical damage stimulating release of chemokines that diffuse from the injury site. These data strongly suggest that chemokines are instrumental in the initiation of repair processes following brain injury.

Beta-adrenergic drug induced hyperplasia in the immature rat parotid and submandibular glands.

In this study the proliferative response of rat parotid (PRG) and submandibular (SMG) gland acinar cells to beta-adrenergic stimulation with Isoproterenol (a non-selective beta-agonist) or terbutaline (a relatively selective beta 2-agonist) was determined during the 4th-5th postnatal weeks in intact and guanethidine-sympathectomized (Sx) rats. Rats were divided into 2 age groups (21 and 28 days) and 6 experimental groups (control-intact (C), guanethidine-treated (Sx), intact + TER (C + TER), intact + Isoproterenol (C + IPR), guanethidine-treated + TER (Sx + TER), and guanethidine-treated + isoproterenol (Sx + IPR]. Intact and Sx rats were treated with either IPR or TER for 3 days (days 21, 22, and 23 or days 28, 29 and 30). On day 24 or 31 all rats were injected with [3H]-thymidine and killed 1 h later. PRG of Sx and C + TER rats showed no significant differences from controls in wet weight while SMG from Sx rats demonstrated a reduced wet weight compared to C rats. [3H]Thymidine labelling index and mitotic index were not significantly different in Sx and C + TER rats in either PRG or SMG. C + IPR rats showed increased wet weight, labelling and mitotic index compared to controls (P less than 0.01). Sx + IPR increased values over controls (P less than 0.01) and above C + IPR values (P less than 0.01). Sx + TER values were significantly higher than controls.(ABSTRACT TRUNCATED AT 250 WORDS)