Determination of toxic and essential metals in rock and sea salts using pulsed nanosecond laser-induced breakdown spectroscopy.

A spectrometer based on pulsed nanosecond laser-induced breakdown spectroscopy (LIBS) was employed for the quantitative determination of heavy and essential metals in salts from various sources available in Pakistan. Six salt samples were collected from sea salt and rock salt. Toxic metals (Cu, Cd, and Ni) and other microessentials (Fe, Ca, Co, Mg, Mn, S, and Zn) were investigated from the recorded spectra. The detection system was calibrated using a parametric dependence study. The quantitative analyses were accomplished under the assumption of local thermodynamic equilibrium and optically thin plasma. The results by the LIBS technique were in agreement with the outcomes of the same samples studied using a more standard approach like inductively coupled plasma-atomic emission spectroscopy (ICP-AES). When the concentrations of heavy and essential metals were calculated using a calibration-free LIBS method that does not need a standard salt specimen and dilution, both LIBS and ICP-AES were also in good agreement. The limit of detection of the experimental set up was determined for the observed heavy metals in the studied samples.

Controlling scabies in madrasahs (Islamic religious schools) in Bangladesh.

OBJECTIVES: To assess the effectiveness of a scabies control programme in reducing the prevalence of scabies in urban Bangladesh madrasahs, where the condition is extremely common. STUDY DESIGN: A controlled trial involving four intervention madrasahs (total students 2359) and four control madrasahs (total students 2465) in Dhaka Metropolitan Area. METHODS: A baseline scabies sample survey was carried out on 40 and 44 students of four intervention and four control madrasahs, respectively. Another 40 students of the intervention madrasahs were administered a pre-intervention test on scabies knowledge. This was followed by mass treatment of all students, teachers and staff of the eight madrasahs with topical 5% permethrin cream. The subsequent intervention involved daily monitoring of students for five key personal hygiene practices, weekly 10-min scabies health education classes, supply of simple and inexpensive products to students to prevent cross-infestation to/from peers (e.g. plastic bags, clothes hangers), and chemotherapy of new students detected with scabies. After 4 months of the intervention, the prevalence of scabies, personal hygiene practices and scabies knowledge were assessed in students of the intervention madrasahs. RESULTS: Before the intervention, the prevalence of scabies was 61% and 62% in intervention and control madrasahs, respectively (P = 1.00). After mass scabies treatment in all eight madrasahs and 4 months of intervention, the prevalence of scabies was reduced to 5% and 50% in intervention and control madrasahs, respectively (P < 0.001). There were significant improvements in all five personal hygiene practices at the intervention madrasahs. Mean test scores for scabies knowledge were 40% before the intervention and 99% after the intervention in the four intervention madrasahs. The cost of this programme was US$1.60 per student, and primarily included products such as plastic bags and clothes hangers, and health education material. CONCLUSIONS: This programme demonstrates a pragmatic and cost-effective way to control scabies in a residential institutional setting. It is recommended that this programme should be scaled up to all residential madrasahs in Bangladesh.

Boundary spanning at the science-policy interface: the practitioners' perspectives.

Cultivating a more dynamic relationship between science and policy is essential for responding to complex social challenges such as sustainability. One approach to doing so is to "span the boundaries" between science and decision making and create a more comprehensive and inclusive knowledge exchange process. The exact definition and role of boundary spanning, however, can be nebulous. Indeed, boundary spanning often gets conflated and confused with other approaches to connecting science and policy, such as science communication, applied science, and advocacy, which can hinder progress in the field of boundary spanning. To help overcome this, in this perspective, we present the outcomes from a recent workshop of boundary-spanning practitioners gathered to (1) articulate a definition of what it means to work at this interface ("boundary spanning") and the types of activities it encompasses; (2) present a value proposition of these efforts to build better relationships between science and policy; and (3) identify opportunities to more effectively mainstream boundary-spanning activities. Drawing on our collective experiences, we suggest that boundary spanning has the potential to increase the efficiency by which useful research is produced, foster the capacity to absorb new evidence and perspectives into sustainability decision-making, enhance research relevance for societal challenges, and open new policy windows. We provide examples from our work that illustrate this potential. By offering these propositions for the value of boundary spanning, we hope to encourage a more robust discussion of how to achieve evidence-informed decision-making for sustainability.

Apoptosis and expression of Bcl-2 after compression trauma to rat spinal cord.

We have evaluated by in situ nick-end labeling the presence of apoptotic cells in the spinal cord of rats with compression injury at the level of Th8-9 of mild, moderate, and severe degrees resulting in no neurologic deficit, reversible paraparesis, and paraplegia, respectively. Rats with compression injury surviving 4 or 9 days showed apoptotic glial cells in the longitudinal tracts of the Th8-9, the cranial Th7, and the caudal Th10 segments. The apoptotic cells were most frequently observed in Th7. They did not express glial fibrillar acidic protein (GFAP) and their morphology was compatible with that of oligodendrocytes. Neurons of the gray matter did not present signs of apoptosis. In addition, we studied the immunohistochemical expression of Bcl-2, an endogenous inhibitor of apoptosis. Compression induced Bcl-2 immunoreactivity in axons of the long tracts, particularly after moderate and severe compression and 1-day survival. Neurons of dorsal root ganglia were immunoreactive but the neurons of the spinal cord were unstained. The accumulation, presumably caused by arrested axonal transport in sensory pathways, was absent in rats surviving 9 days. In conclusion, compression trauma to rat spinal cord induces signs of apoptosis in glial cells, presumably oligodendrocytes of the long tracts. This may induce delayed myelin degeneration after trauma to the spinal cord. Bcl-2 does not seem to be upregulated in oligodendrocytes.

Expression of the ubiquitin carboxyl-terminal hydrolase PGP 9.5 in axons following spinal cord compression trauma. An immunohistochemical study in the rat.

Protein gene product 9.5 (PGP 9.5) is a neuron-specific protein which acts as a ubiquitin carboxyl-terminal hydrolase. It facilitates the conversion of polyubiquitin to monoubiquitin, which can be reused for another catalytic cycle. Monoubiquitin plays an important role in degrading abnormal and denatured proteins. Previously, we have reported that ubiquitin-like immunoreactivity is expressed in axonal swellings following compression trauma to the rat thoracic cord. It was characterized by fast occurrence, progressive increase and gradual disappearance over a period of 9 days. The expression of PGP 9.5 has now been studied in the same material. Control rats showed a weak PGP 9.5 immunoreactivity in the nerve cell bodies of the cord. Except for the corticospinal tracts, the axons of other longitudinal tracts were weakly stained. Accumulation of PGP 9.5 immunoreactivity occurred in expanded axons at the site of compression already 4 h after trauma. They became more frequent in number 1 and 4 days after injury and remained so over the entire observation period of 9 days. The labelled axons were randomly distributed in the longitudinal tracts, but were never found in the corticospinal tracts. The extent of immunoreactivity was related to the degree of impact on the cord. Compression injury thus induces accumulation of both ubiquitin and PGP 9.5 immunoreactivity in axonal expansions. The injured axons may have a mechanism for degradation of proteins by the ubiquitin-mediated proteolytic pathway and another mechanism for effective ubiquitin regenerative cycling by the action of PGP 9.5.

MAP2 and neurogranin as markers for dendritic lesions in CNS injury. An immunohistochemical study in the rat.

We compared two staining methods for the demonstration of dendrites under normal and pathological conditions of the rat central nervous system. MAP2- and neurogranin immunohistochemistry was applied to samples from normal tissue, spinal cord subjected to graded compression trauma, cerebral cortex following contusion trauma, and brains with focal ischemic lesions induced by occlusion of the middle cerebral artery (MCAO). Normal rats showed MAP2 immunoreactivity in nerve cell bodies and dendrites of brain and spinal cord. However, neurogranin staining was present only in nerve cell bodies and dendrites of the normal brain, and not in the spinal cord. Reduction of MAP2 immunoreactivity was seen in lesions of spinal cords subjected to compression trauma. Neurogranin staining was of no value in this experimental condition since it was not present under normal conditions. The brain contusions showed loss of both MAP2- and neurogranin immunoreactivity at the site of the lesion. MCAO resulted in an extensive loss of MAP2- and neurogranin staining in the ipsilateral hemisphere. In conclusion, our study shows that MAP2 immunostaining is a sensitive method for identifying dendritic lesions of various CNS injuries in the rat. Neurogranin immunostaining is an alternative method for investigations of dendritic pathology in the brain but not in the spinal cord.

Improved recovery after spinal cord injury in neuronal nitric oxide synthase-deficient mice but not in TNF-alpha-deficient mice.

Wild-type mice and mice lacking nitric oxide synthase (NOS) of neuronal type or TNF-alpha were subjected to an extradural compression of the thoracic spinal cord. The functional outcome of the hind limbs was assessed by using a motor function score (MFS). The injury resulted in paraplegia of the hind limbs in wild-type mice at day 1 after injury. Gradual recovery was observed during the following 14 days. Injured NOS -/- animals had an improved hind limb motor function during the entire observation period compared to wild-type controls. The difference was statistically significant on day 10 (p < 0.022) and day 14 (p < 0.048) after injury. At the site of injury, there was a trend of gray matter preservation in NOS -/- mice, as measured by MAP2 staining (p < 0.077). Injured mice lacking TNF-alpha had the lowest motor score among all the groups on day 1. During the following period, they had motor scores similar to those of wild-type controls and there was no significant difference at any time point. TNF-alpha -/- animals showed a trend of decreased white matter preservation compared to wild-type animals (p < 0.097). Our study shows that after spinal cord injury, mice lacking NOS have a better functional ability of their hind limbs than controls with the same degree of injury. This would indicate that the functional outcome is influenced in a negative way in wild mice by the presence of NO. The degree of secondary damage to the spinal cord might be attenuated in NOS-deficient mice.

Spinal cord injury in ICAM-1-deficient mice: assessment of functional and histopathological outcome.

Adhesion molecule-mediated adhesion and extravasation of leukocytes may constitute a mechanism of secondary tissue damage following spinal cord injury (SCI). The objective of the present study was to determine to what extent genetic deficiency in the adhesion molecule ICAM-1 influences functional and histopathological measures of outcome following SCI. ICAM-1-/- (n = 11) and wild-type (n = 9) mice were subjected to a compression-type SCI. Assessment of hind-limb motor function was done on days 1, 2, 4, 7, 10, and 14 after injury, using a motor function scoring system. Injury resulted in a drastically impaired hind limb motor function at day one after injury followed by a partial recovery during the observation period. No significant functional differences were found between the experimental groups at any time-point. Fourteen days after injury the animals were sacrificed and the spinal cords were processed for histopathological and immunohistochemical evaluation. Luxol-stained, MAP2-, GFAP- and iba-1-immunostained cross-sectional areas were quantitated using a computerized image analysis system to investigate white matter damage, neuronal loss, astrocytic response and microglial activation respectively. None of these parameters differed significantly between the groups. Separate experiments revealed that the early (24 h postinjury) infiltration of polymorphonuclear leukocytes was significantly reduced in white matter but not in the grey matter of ICAM-1-/- mice, compared to injured controls. In summary, these results do not support the concept that ICAM-1 alone mediates secondary tissue damage following traumatic SCI in the mouse.

Pretreatment with alpha-phenyl-N-tert-butyl-nitrone (PBN) improves energy metabolism after spinal cord injury in rats.

We evaluated in rats, the effect of the spin trap alpha-phenyl-N-tert-butyl nitrone (PBN) on energy metabolism after severe spinal cord injury (SCI). A laminectomy of vertebrae Th7 and Th8 was made. A probe was inserted in a dorsal horn, and microdialysis was performed for 1.5 h before and 4 h after applying severe compression (4.5 g/mm2) for 5 min. Thirty minutes before trauma 30-mg/kg PBN or saline was given intravenously and a second dose of 10 mg/kg after 3 h. Microdialysis samples were collected at intervals of 10 min and analysed by high performance liquid chromatography. As reported previously there was a severalfold rise of lactate after trauma. The mean level of lactate was consistently lower in animals pretreated with PBN, but the difference was statistically significant between the groups only at 200 min after trauma. Lactate normalized more rapidly in PBN pretreated animals. In saline-treated rats, hypoxanthine quickly rose and reached a maximum 23 times above basal level 20 min after trauma, while the rise was 14 times in PBN pretreated rats. The increase of hypoxanthine was significantly lower and normalized more rapidly in PBN pretreated animals. This study suggests that PBN pretreatment attenuates lactic acidosis and improves energy metabolism after severe SCI. The effect may, at least partly, reflect amelioration of radical induced mitochondrial dysfunction.

Astrocytic reaction after graded spinal cord compression in rats: immunohistochemical studies on glial fibrillary acidic protein and vimentin.

The relation between the degree of spinal cord compression and the extent of early posttraumatic reaction of astrocytes was investigated in rats using the blocking-weight technique to induce a spinal cord compression at the level of the Th8-9. Immunohistochemistry was used to detect changes in the expression of glial fibrillary acidic protein (GFAP) and vimentin up to 24 h after injury. A mild compression, which did not cause any measurable neurological deterioration, induced a mild increase of GFAP immunoreactivity at 4 h and a more marked and widespread immunoreactivity at 24 h. The greatest increase of GFAP immunoreactive astrocytes occurred in rats with moderate compression of the cord causing reversible paraparesis and in animals with severe compression leading to paraplegia. The increase of GFAP immunoreactivity was present already 4 h after injury in virtually all the segments investigated (Th5-6-Th11-12) and was most marked at 24 h. Vimentin immunoreactivity of control rats was present in the ependymal cells of the central canal, the leptomeninges, and walls of a few intramedullary vessels. Occasional astrocytes were stained. In rats surviving 24 h after moderate and severe compression vimentin immunoreactivity was increased in the walls of intramedullary blood vessels including capillaries of one rostral and one caudal segment. Many macrophages with immunoreactivity appeared and occasional glial cells with astrocyte shape were stained. This investigation shows that within 24 h after compression of the spinal cord a widespread astrocyte reaction occurs. Even a mild compression that does not produce any signs of motor dysfunction can induce widespread astrocyte alterations in the spinal cord. This astrocyte response is more marked in rats with more severe compression leading to more pronounced neurological deterioration. The increase in vimentin immunoreactivity of blood vessels is more localized and occurs in moderate and severe compression of the cord.

Changes of extracellular levels of amino acids after graded compression trauma to the spinal cord: an experimental study in the rat using microdialysis.

We evaluated in rats, the time course of changes in extracellular levels of amino acids, lactate and pyruvate, which ensued spinal cord compression of mild, moderate, and severe degrees. The neurochemical findings measured by HPLC were compared with known outcome measures of this model. A laminectomy of vertebrae Th7 and Th8 was made and a microdialysis probe was inserted in one dorsal horn. Fluid samples were collected at intervals of 10 min. Dialysate lactate and lactate/pyruvate ratios increased in proportion to the severity of injury, suggesting a progressive derangement of energy metabolism. Mild trauma, with no neurologic deficits, did not induce any remarkable change of amino acids, but taurine values were temporarily slightly elevated. Moderate trauma, leading to transient paraparesis, resulted in a transient rise of glutamate and taurine. Severe trauma resulting in paraplegia of the hind limbs induced profound changes of extracellular amino acids. Glutamate and aspartate rose 5-6 times above basal level. There were marked elevations of taurine, glycine, arginine, alanine, asparagine, histidine, serine, threonine, and tyrosine after this degree of trauma. Glutamate, aspartate, and taurine returned to the basal level within 50 min, whereas most of the other amino acids remained elevated throughout the experiment. Thus, we found profound disturbances of extracellular amino acids and energy metabolites. The elevations of glutamate and aspartate correlated with previously recorded data on neurological outcome. The composition of the early extracellular edema showed marked temporal changes related to the severity of impact. Future studies regarding treatment of traumatic edema should focus on its chemical composition as well as its volume since such edema is not uniform in composition.

Effects of moderate hypothermia on extracellular lactic acid and amino acids after severe compression injury of rat spinal cord.

We evaluated in rats, the effect of moderate hypothermia (30-31 degrees C) on extracellular levels of amino acids, with special emphasis on the excitatory amino acids (EAAs) glutamate and aspartate, lactate and pyruvate, after severe spinal cord compression. A laminectomy of Th7 and Th8 was made. A probe was inserted in a dorsal horn and microdialysis was performed for 1.5 h before and 4 h after applying severe compression for 5 min. Dialysate samples were collected at intervals of 10 min and analyzed by high-performance liquid chromatography. In normothermic (37.5 degrees C) animals there was a several-fold rise of glutamate that peaked in the first 10 min fraction after trauma. Hypothermic animals showed a similar increase after trauma, which was statistically significant until 20 min after injury. The level of glutamate was significantly higher in hypothermic animals from 20 to 70 min after injury, compared with normothermic animals. Aspartate also showed a marked increase following injury. The peak concentration was similar for both groups, whereas recovery was delayed in hypothermic animals. There was no significant difference between the normothermic and hypothermic animals for arginine, taurine, alanine, glutamine, histadine, glycine, threonine, tyrosine, and asparagine. No significant effect of hypothermia on lactate or lactate/pyruvate was noted. However, the mean level of lactate tended to be lower and recovery was quicker in hypothermic animals. The results of the present study suggest that moderate hypothermia does not attenuate extracellular accumulation of EAAs or markedly improve energy metabolism in our model. Instead, our findings raise the possibility that moderate hypothermia prolongs the duration of glutamate receptor overactivation. Since hypothermia effectively attenuates glutamate release in CNS and spinal cord ischemia models our results suggest different mechanisms of extracellular accumulation of EAAs in ischemia and trauma.

Systemic hypothermia after spinal cord compression injury in the rat: does recorded temperature in accessible organs reflect the intramedullary temperature in the spinal cord?

This article addresses one basic issue regarding the use of systemic hypothermia in the acute management of spinal cord injury, namely, how to interpret temperature recordings in accessible organs such as the rectum or esophagus with reference to the spinal cord temperature. Thirty-six rats, divided into six groups, were randomized to laminectomy or to severe spinal cord compression trauma, and were further randomized to either a cooling/rewarming procedure or continuous normothermia (esophageal temperature 38 degrees C) for 90 min. The first procedure comprised normothermia during the surgical procedure, followed by lowering of the esophageal temperature from 38 degrees C to 30 degrees C (the hypothermic level), a 20-min steady-state period at 30 degrees C, rewarming to 38 degrees C, and finally a 20-min steady-state period at 38 degrees C. The esophageal, rectal, and epidural temperatures were recorded in all animals. The intramedullary temperature was also recorded invasively in four of the six groups. We conclude that the esophageal temperature is safe and easy to record and, in our setting, reflects the epidural temperature. The differences registrated may reflect a true deviation of the intramedullary temperature due to initial environmental exposure and secondary injury processes. Our results indicate that the esophageal temperature exceeds the intramedullary temperature during the initial recording and final steady state following rewarming, but not during the most crucial part of the experiment, the hypothermic period. The core temperature measured in the esophagus can therefore be used to evaluate the intramedullary temperature during alterations of the systemic temperature and during hypothermic periods.

Expression of ICAM-1 and CD11b after experimental spinal cord injury in rats.

We have performed an immunohistochemical study on the expression of the adhesion molecules ICAM-1 and CD11b 1 h to 1 week following a compression injury to the rat spinal cord. The spinal cord of control animals showed ICAM-1 expression in some vessels and in the leptomeninges. Mechanical compression of the spinal cord induced an endothelial upregulation of ICAM-1 that was maximal in rats surviving 1-2 days after injury. This reaction was seen at the center of the lesion as well as in the perifocal zones. Apart from the endothelial upregulation, increased ICAM-1 expression also was found in leptomeningeal and ependymal cells of traumatized animals. In control animals resting microglial cells were moderately CD11b immunoreactive. Trauma induced a rapid microglial upregulation of CD11b in the white matter that was evident even at 1 h after injury. By 1 day to 1 week posttrauma conformational changes consistent with microglial activation, i.e., transformation into phagocytic microglial cells, were seen in the white matter. In the gray matter, CD11b immunohistochemistry revealed massive infiltration of phagocytic microglial cells and macrophages in animals surviving 1 day to 1 week. Intravascular and infiltrating leukocytes were intensely CD11b immunopositive. As reflected by CD11b immunohistochemistry, the maximal infiltration of polymorphonuclear leukocytes occurred at 2 days after the insult. Endothelial upregulation of ICAM-1 facilitates adhesion and extravasation of leukocytes by binding to the counterreceptor CD11b. Knowledge regarding the expression and cellular distribution of such molecules after central nervous system trauma is important since inflammatory mechanisms have been suggested to be involved in secondary neurological damage and thus constitute potential targets of therapy.

Changes of beta-amyloid precursor protein after compression trauma to the spinal cord: an experimental study in the rat using immunohistochemistry.

We evaluated by immunohistochemistry the changes of beta-amyloid precursor protein (beta APP) and beta-amyloid peptide (beta A) in the spinal cord of rats with compression injury at Th8-9 of mild, moderate, and severe degrees. The spinal cord of normal rats and animals with laminectomy revealed immunoreactivity to beta APP in nerve cell bodies, the initial part of a few axons of the gray matter, and in scattered glial cells. At 4 h after compression, beta APP-immunoreactivity occurred in a few swollen axons of the longitudinal tracts; such beta APP-immunoreactive axons remained throughout the experimental period of 9 days. The number of immunoreactive axons and the intensity of their immunoreactivity were increased in rats with moderate and severe compression. The caudal Th10 segment exhibited more pronounced accumulation of beta APP immunoreactivity than the cranial Th segment. There was no evidence of beta A accumulation after compression injury. In conclusion, there is a rapidly occurring, long-lasting accumulation of immunoreactive beta-amyloid precursor protein after compression injury of rat spinal cord. This accumulation is related to the degree of impact to the cord.

Microtubule-associated protein 2 as a sensitive marker for dendrite lesions after spinal cord trauma: an immunohistochemical study in the rat.

We evaluated, by irnmunohistochemistry, the changes of microtubule-associated protein 2 (MAP2) of rat spinal cord following compression injury of mild, moderate and severe degrees at the Th8-9 level. The spinal cord of normal rats and animals subjected to laminectomy only, presented immunoreactivity to MAP2 in nerve cell bodies and dendrites but not in axons and other structures. Following moderate and severe compression resulting in reversible paraparesis or irreversible paraplegia, respectively, the compressed segment showed loss of MAP2 immunoreactivity in dendrites and nerve cell bodies already 4 h after injury. This phenomenon remained throughout the experimental period of 9 days. Our findings indicate that there is a rapid and long-lasting reduction of MAP2 in nerve cell bodies and dendrites of the compressed segment and that this alteration is related to the degree of the impact to the cord. The reduction of MAP2 may well have functional implications by interfering with neurotransmission. MAP2 immuno-staining is an excellent way of studying dendritic changes in spinal cord trauma and can be used in future experiments designed to investigate the influence of various therapeutic measures on secondary lesions after trauma.

Improved recovery after spinal cord trauma in ICAM-1 and P-selectin knockout mice.

Traumatic spinal cord injury is followed by infiltration of leukocytes, influenced by endothelial adhesion molecules such as ICAM-1 and P-selectin. In order to evaluate the pathogenetical role of these molecules, wild-type mice and mice lacking ICAM-1 and P-selectin were subjected to an experimental spinal cord compression of two degrees of severity. Hind limb motor function decreased after injury in all animals but the groups of injured ICAM-1/P-selectin knockout animals had a better functional outcome during the entire observation period of 14 days. This difference was statistically significant on day 1. Our results indicate that adhesion molecules influence the functional outcome after spinal cord injury in a negative way and may be a target for future therapy of neurotrauma.

Effects of alpha-phenyl-N-tert-butyl nitrone (PBN) on compression injury of rat spinal cord.

alpha-Phenyl-N-tert-butyl Nitrone (PBN) is a free radical scavenger which recently has proved to be neuroprotective in experimental studies on focal cerebral ischemia and infarction. We therefore studied the effect of this drug in a model of moderate compression injury to rat spinal cord at the midthoracic level. The compound was given intraperitoneally 0.5 h before (100 mg/kg b.w) and at 1.5 h (50 mg/kg b.w) and 3.5 h (50 mg/kg b.w) after compression. Treated animals and controls (vehicle alone) were allowed to survive for 1 or 9 days following trauma. The functional outcome was tested by the inclined plane method and the motor performance score. By using MAP2 immunostaining the number of nerve cell bodies in the ventral horn and the ratio of MAP2 immunostained area to area of whole section of the cord were assessed to detect loss of neurons and loss of dendrites in the compressed segment. beta APP and PGP9.5 immunostaining was used to demonstrate axonal lesions. Treated and control rats showed at day 1 when tested with the inclined plane method a marked reduction of the capacity angle. This abnormality recovered gradually over the following days and was normalized at day 9. The motor performance score showed a marked reduction at day 1 which almost normalized at day 9. There was no difference regarding the functional outcome between rats given PBN and controls in none one of these functional tests. The spinal cord of normal rats presented immunoreactivity to MAP2 in nerve cell bodies and dendrites but not in axons and other structures. Following compression there was at day 1 and 9 a marked loss of MAP2 immunoreactivity in dendrites and nerve cell bodies. We could not detect any difference between the PBN and the control rats regarding the degree of cell loss or degree of reduction of dendrite staining. No difference between the two groups was seen with the axonal immunostainings (beta APP and PGP9.5). In conclusion, our study did not reveal any neuroprotective effect of PBN on the functional outcome and morphology (immunostaining to MAP2, beta APP and PGP9.5) in this model of moderate compression trauma to rat spinal cord.

Macrodactyly.

We report the results of the treatment of 23 patients with macrodactyly. Eighteen had a two-stage bulk-reducing (defatting) procedure; phalangectomy was used to shorten the digits. At a mean follow-up of nine years (2 to 12), two patients had been lost to follow-up, and three await a second-stage procedure. Good cosmetic correction was achieved in 12 patients, with satisfactory results in seven; two patients had poor results and required amputation.

Resurfacing of skin in hand injuries.

The Authors discuss their experience with the use of various flaps (radial artery, groin and abdomen) in the primary or delayed cover of skin defect in the hand, in a total number of 20 cases. All the three types of flaps took up well in 3-4 weeks with minimal complications. The Authors preferred the radial artery flap to the groin and abdominal flaps, in that order.