Double screw versus angular stable plate fixation of scaphoid waist nonunions in combination with intraoperative extracorporeal shockwave therapy (ESWT).

INTRODUCTION: Over the past years, different fixation techniques focused on rotational stability in order to increase stability and stimulate union rates. Additionally, extracorporeal shockwave therapy (ESWT) has gained importance in the treatment of delayed and nonunions. Purpose of this study was to compare the radiological and clinical outcome of two headless compression screws (HCS) and plate fixation in scaphoid nonunions, in combination with intraoperative high energy ESWT. MATERIALS AND METHODS: Thirty-eight patients with scaphoid nonunions were treated by using a nonvascularized bone graft from the iliac crest and stabilization with either two HCS or a volar angular stable scaphoid plate. All patients received one ESWT session with 3000 impulses and energy flux per pulse of 0.41 mJ/mm2 intraoperatively. Clinical assessment included range of motion (ROM), pain according to the Visual Analog Scale (VAS), grip strength, disability of the Arm Shoulder and Hand Score, Patient-Rated Wrist Evaluation Score, Michigan Hand Outcomes Questionnaire and modified Green O'Brien (Mayo) Wrist Score. To confirm union, a CT scan of the wrist was performed. RESULTS: Thirty-two patients returned for clinical and radiological examination. Out of these, 29 (91%) showed bony union. All patients treated with two HCS compared to 16 out of 19 (84%) patients treated by plate showed bony union on the CT scans. The difference was not statistically significant. However, at a mean follow-up interval of 34 months, no significant differences could be found in ROM, pain, grip strength and patient-reported outcome measurements between the two HCS and plate group. Height-to-length ratio and capitolunate angle improved significantly in both groups compared to preoperative. CONCLUSIONS: Scaphoid nonunion stabilization by using two HCS or angular stable volar plate fixation and intraoperative ESWT results in comparable high union rates and good functional outcome. Due to the higher rate for a secondary intervention (plate removal), HCS might be preferable as first choice, whereas the scaphoid plate fixation should be reserved for recalcitrant (substantial bone loss, humpback deformity or failed prior surgical intervention) scaphoid nonunions.

Reducing False Alarm Rates in Neonatal Intensive Care: A New Machine Learning Approach.

In neonatal intensive care units (NICUs), 87.5% of alarms by the monitoring system are false alarms, often caused by the movements of the neonates. Such false alarms are not only stressful for the neonates as well as for their parents and caregivers, but may also lead to longer response times in real critical situations. The aim of this project was to reduce the rates of false alarms by employing machine learning algorithms (MLA), which intelligently analyze data stemming from standard physiological monitoring in combination with cerebral oximetry data (in-house built, OxyPrem). MATERIALS & METHODS: Four popular MLAs were selected to categorize the alarms as false or real: (i) decision tree (DT), (ii) 5-nearest neighbors (5-NN), (iii) naïve Bayes (NB) and (iv) support vector machine (SVM). We acquired and processed monitoring data (median duration (SD): 54.6 (± 6.9) min) of 14 preterm infants (gestational age: 26 6/7 (± 2 5/7) weeks). A hybrid method of filter and wrapper feature selection generated the candidate subset for training these four MLAs. RESULTS: A high specificity of >99% was achieved by all four approaches. DT showed the highest sensitivity (87%). The cerebral oximetry data improved the classification accuracy. DISCUSSION & CONCLUSION: Despite a (as yet) low amount of data for training, the four MLAs achieved an excellent specificity and a promising sensitivity. Presently, the current sensitivity is insufficient since, in the NICU, it is crucial that no real alarms are missed. This will most likely be improved by including more subjects and data in the training of the MLAs, which makes pursuing this approach worthwhile.

TLR4 inhibitor TAK-242 attenuates the adverse neural effects of diet-induced obesity.

BACKGROUND: Obesity exerts negative effects on brain health, including decreased neurogenesis, impaired learning and memory, and increased risk for Alzheimer's disease and related dementias. Because obesity promotes glial activation, chronic neuroinflammation, and neural injury, microglia are implicated in the deleterious effects of obesity. One pathway that is particularly important in mediating the effects of obesity in peripheral tissues is toll-like receptor 4 (TLR4) signaling. The potential contribution of TLR4 pathways in mediating adverse neural outcomes of obesity has not been well addressed. To investigate this possibility, we examined how pharmacological inhibition of TLR4 affects the peripheral and neural outcomes of diet-induced obesity. METHODS: Male C57BL6/J mice were maintained on either a control or high-fat diet for 12 weeks in the presence or absence of the specific TLR4 signaling inhibitor TAK-242. Outcomes examined included metabolic indices, a range of behavioral assessments, microglial activation, systemic and neuroinflammation, and neural health endpoints. RESULTS: Peripherally, TAK-242 treatment was associated with partial inhibition of inflammation in the adipose tissue but exerted no significant effects on body weight, adiposity, and a range of metabolic measures. In the brain, obese mice treated with TAK-242 exhibited a significant reduction in microglial activation, improved levels of neurogenesis, and inhibition of Alzheimer-related amyloidogenic pathways. High-fat diet and TAK-242 were associated with only very modest effects on a range of behavioral measures. CONCLUSIONS: These results demonstrate a significant protective effect of TLR4 inhibition on neural consequences of obesity, findings that further define the role of microglia in obesity-mediated outcomes and identify a strategy for improving brain health in obese individuals.

Interactions between inflammation, sex steroids, and Alzheimer's disease risk factors.

Alzheimer's disease (AD) is an age-related neurodegenerative disorder for which there are no effective strategies to prevent or slow its progression. Because AD is multifactorial, recent research has focused on understanding interactions among the numerous risk factors and mechanisms underlying the disease. One mechanism through which several risk factors may be acting is inflammation. AD is characterized by chronic inflammation that is observed before clinical onset of dementia. Several genetic and environmental risk factors for AD increase inflammation, including apolipoprotein E4, obesity, and air pollution. Additionally, sex steroid hormones appear to contribute to AD risk, with age-related losses of estrogens in women and androgens in men associated with increased risk. Importantly, sex steroid hormones have anti-inflammatory actions and can interact with several other AD risk factors. This review examines the individual and interactive roles of inflammation and sex steroid hormones in AD, as well as their relationships with the AD risk factors apolipoprotein E4, obesity, and air pollution.

[Relevance of personal contextual factors of the ICF for use in practical social medicine and rehabilitation]. / Bedeutung der personbezogenen Faktoren der ICF für die Nutzung in der praktischen Sozialmedizin und Rehabilitation.

Personal contextual factors play an essential part in the model of the International Classification of Functioning, Disability and Health (ICF). The WHO has not yet classified personal factors for global use although they impact on the functioning of persons positively or negatively. In 2010, the ICF working group of the German Society of Social Medicine and Prevention (DGSMP) presented a proposal for the classification of personal factors into 72 categories previously arranged in 6 chapters. Now a positioning paper has been added in order to stimulate a discussion about the fourth component of the ICF, to contribute towards a broader and common understanding about the nature of personal factors and to incite a dialogue among all those involved in health care as well as those people with or with-out health problems in order to gain a comprehensive perspective about a person's condition.

Multi-lineage heart-chip models drug cardiotoxicity and enhances maturation of human stem cell-derived cardiovascular cells.

Cardiovascular toxicity causes adverse drug reactions and may lead to drug removal from the pharmaceutical market. Cancer therapies can induce life-threatening cardiovascular side effects such as arrhythmias, muscle cell death, or vascular dysfunction. New technologies have enabled cardiotoxic compounds to be identified earlier in drug development. Human induced pluripotent stem cell (hiPSC)-derived cardiomyocytes (CMs) and vascular endothelial cells (ECs) can screen for drug-induced alterations in cardiovascular cell function and survival. However, most existing hiPSC models for cardiovascular drug toxicity utilize two-dimensional, immature cells grown in static culture. Improved in vitro models to mechanistically interrogate cardiotoxicity would utilize more adult-like, mature hiPSC-derived cells in an integrated system whereby toxic drugs and protective agents can flow between hiPSC-ECs that represent systemic vasculature and hiPSC-CMs that represent heart muscle (myocardium). Such models would be useful for testing the multi-lineage cardiotoxicities of chemotherapeutic drugs such as VEGFR2/PDGFR-inhibiting tyrosine kinase inhibitors (VPTKIs). Here, we develop a multi-lineage, fully-integrated, cardiovascular organ-chip that can enhance hiPSC-EC and hiPSC-CM functional and genetic maturity, model endothelial barrier permeability, and demonstrate long-term functional stability. This microfluidic organ-chip harbors hiPSC-CMs and hiPSC-ECs on separate channels that can be subjected to active fluid flow and rhythmic biomechanical stretch. We demonstrate the utility of this cardiovascular organ-chip as a predictive platform for evaluating multi-lineage VPTKI toxicity. This study may lead to the development of new modalities for the evaluation and prevention of cancer therapy-induced cardiotoxicity.

Human iPSC-derived neural progenitor cells secreting GDNF provide protection in rodent models of ALS and retinal degeneration.

Human induced pluripotent stem cells (iPSCs) are a renewable cell source that can be differentiated into neural progenitor cells (iNPCs) and transduced with glial cell line-derived neurotrophic factor (iNPC-GDNFs). The goal of the current study is to characterize iNPC-GDNFs and test their therapeutic potential and safety. Single-nuclei RNA-seq show iNPC-GDNFs express NPC markers. iNPC-GDNFs delivered into the subretinal space of the Royal College of Surgeons rodent model of retinal degeneration preserve photoreceptors and visual function. Additionally, iNPC-GDNF transplants in the spinal cord of SOD1G93A amyotrophic lateral sclerosis (ALS) rats preserve motor neurons. Finally, iNPC-GDNF transplants in the spinal cord of athymic nude rats survive and produce GDNF for 9 months, with no signs of tumor formation or continual cell proliferation. iNPC-GDNFs survive long-term, are safe, and provide neuroprotection in models of both retinal degeneration and ALS, indicating their potential as a combined cell and gene therapy for various neurodegenerative diseases.

Bone metabolism in patients with primary hyperparathyroidism before and after surgery.

Primary hyperparathyroidism (PHPT) is accompanied with a reduced bone mineral density (BMD) and an increased risk of fracture. Surgery is the only option for cure. It is hypothesized that in patients with PHPT bone metabolism normalizes after parathyroidectomy (PTX) and that BMD gradually increases. Fifty-two patients with PHPT who underwent surgery were prospectively followed for 1 year. Biochemical analyses were performed at baseline and 1, 4, 7 days; 6 weeks; and 3, 6, and 12 months, and BMD before and one year after surgery. Parathyroid hormone (PTH), calcium, and the bone resorption marker dropped immediately, but transiently after PTX, bone formation decreased more slowly. Osteoprotegerin (OPG) as well as cathepsin K did not show significant changes. BMD of the lumbar spine, but not of the femoral neck, increased significantly within one year after surgery. Moderate correlations existed between the changes of total calcium, ionized calcium, as well as bone-specific alkaline phosphatase and changes of the lumbar BMD. Patients who needed postoperative supplementation with calcium and vitamin D had significantly higher PTH levels. Some gender-specific differences in patients with PHPT were observed. In patients with PHPT, males appear to be more severely affected than females. Within the first year after PTX, bone metabolism normalized, and BMD of the lumbar spine increased. Patients who needed a supplementation with calcium and vitamin D after PTX preoperatively had higher serum levels of PTH.

Impacts of a perinatal exposure to manganese coupled with maternal stress in rats: Learning, memory and attentional function in exposed offspring.

The developmental effects of chemicals that co-occur in vulnerable populations with elevated psychological stress are of increasing concern to the public. To investigate these concerns, we developed a rodent model of co-occurring perinatal manipulations and conducted a series of cognitive assessments in male and female offspring. Manganese (Mn), a neurodevelopmental toxicant when exceeding physiological requirements, was delivered in the drinking water (0, 2, or 4 mg Mn/mL) of rats from gestational day (GD) 7 to postnatal day (PND) 22. A variable perinatal stress paradigm was applied to half of the animals from GD13 to PND9. Novel object recognition (NOR), Morris water maze (MWM), differential reinforcement of low-rates procedure (DRL) and cued and uncued choice reaction time (CRT) tests were used to assess cognitive functions in offspring. Mn (4 mg/mL) and stress impaired NOR in adolescent males but facilitated NOR performance in females. However, when stress and Mn were combined these effects were attenuated in both sexes. During training for the DRL, Mn (2 mg/mL) facilitated, while stress impaired, lever press learning in both sexes. Few effects related to the treatments were found on DRL or MWM. During cued CRT, Mn (2 and 4 mg/mL) and stress reduced accuracy in males, while stress and Mn (2 mg/mL) increased anticipatory responding and slowed decision time in both sexes. Stress combined with Mn (2 mg/mL) improved cued accuracy and decision time, and Mn attenuated the effect of stress on anticipatory responding in both sexes. Stress slowed female movement time but when combined with Mn (4 mg/mL) the effect of stress was attenuated. During uncued CRT, except for decision time (which replicated effects observed with the cued task), no other effects of Mn or its combination with stress occurred. Females remained negatively affected by stress in most uncued CRT performance measures, while stressed improved male uncued accuracy. Taken together these data do not support increased cognitive impairment produced by Mn when combined with stress. However, the effects of perinatal stress alone, on these cognitive functions may hinder the detection of effects due to chemical exposures and underscores the need to consider the psychological health and wellbeing of the mother and her environment in risk assessment for developmental neurotoxicity of chemicals.

Microglial transcription profiles in mouse and human are driven by APOE4 and sex.

Apolipoprotein E4 (APOE4) is the strongest genetic risk factor for sporadic Alzheimer's disease (AD). APOE4 is known to affect the function of microglia, but to what extent this gene drives microglial gene expression has thus far not been examined. Using a transgenic mouse model of AD that expresses human APOE, we identify a unique transcriptional profile associated with APOE4 expression. We also show a sex and APOE interaction, such that both female sex and APOE4 drive expression of this gene profile. We confirm these findings in human cells, using microglia derived from induced pluripotent stem cells (iMGL). Moreover, we find that these interactions are driven in part by genes related to metal processing, and we show that zinc treatment has APOE genotype-dependent effects on iMGL. These data identify a sex- and APOE4-associated microglial transcription profile and highlight the importance of considering interactive risk factors such as sex and environmental exposures.

Concentration and persistence of tin in rat brain and blood following dibutyltin exposure during development.

Dibutyltin (DBT), a widely used plastic stabilizer, has been detected in the environment as well as human tissues. Although teratological and developmental effects are well documented, there are no published reports of DBT effects on the developing nervous system. As part of a developmental neurotoxicity study of DBT, tissue samples were periodically collected to determine the distribution of total tin (Sn) in brain and whole blood. Pregnant Sprague-Dawley rats were exposed to 0, 10, or 25 ppm DBT in drinking water from gestational day (GD) 6 to weaning at postnatal day (PND) 21. Beginning on PND 3, half of the litters were directly dosed every 2 to 3 d via oral gavage with 0, 1, or 2.5 mg/kg DBT such that the dose level matched the water concentration (for example, litters with 25 ppm DBT in the water received 2.5 mg/kg). For Sn analysis, brain and blood samples were collected from culled pups on PND2 (males and females pooled), from pups (males and females separately) as well as dams at weaning (PND21), and from adult offspring (males and females) at PND93. Total Sn was quantified using inductively coupled plasma-mass spectroscopy (ICP-MS). At all ages, brain Sn levels were higher than blood. At culling, in the directly dosed pups at weaning, and in dams at weaning, Sn levels in both tissues were linearly related to dose. Weanling pups without direct dosing showed lower levels than either culled pups or dams, indicating that lactational exposure was minimal or negligible even while maternal exposure is ongoing. In the adults, Sn levels persisted in brains of directly dosed rats, and the high-dose females had higher levels than did high-dose males. No Sn was detected in adult blood. Thus, during maternal exposure to DBT in drinking water, Sn is placentally transferred to the offspring, but lactational transfer is minimal, if any. Furthermore, Sn is concentrated in brain compared to blood, and its elimination is protracted, on the order of days to months after exposure ends.

Effects of aging, high-fat diet, and testosterone treatment on neural and metabolic outcomes in male brown Norway rats.

Risk for Alzheimer's disease (AD) is affected by multiple factors, including aging, obesity, and low testosterone. We previously showed that obesity and low testosterone independently and interactively exacerbate AD-related outcomes in young adult rodents. The goals of the present study are two-fold: to examine whether the effects of an obesogenic diet differ with increasing age and to determine if testosterone treatment in middle-aged and aged animals mitigates negative effects of the diet. Male brown Norway rats were maintained on control or high-fat diets for 12 weeks beginning in young adulthood, middle age, or advanced age. Separate cohorts of middle-aged and aged animals were treated with testosterone during dietary manipulations. Endpoints included metabolic indices, inflammation, cognitive performance, and neural health outcomes. Aging was associated with poorer outcomes that were generally exacerbated by high-fat diet, especially at middle age. Testosterone treatment was largely without benefit, exerting only subtle effects on a select number of measures. Understanding how the deleterious effects of obesity are affected by advancing age and the ability of protective strategies such as testosterone to reduce these effects may provide significant insight into both the development and prevention of age-related cognitive decline and AD.

Young bone marrow transplantation preserves learning and memory in old mice.

Restoration of cognitive function in old mice by transfer of blood or plasma from young mice has been attributed to reduced C-C motif chemokine ligand 11 (CCL11) and ß2-microglobulin, which are thought to suppress neurogenesis in the aging brain. However, the specific role of the hematopoietic system in this rejuvenation has not been defined and the importance of neurogenesis in old mice is unclear. Here we report that transplantation of young bone marrow to rejuvenate the hematopoietic system preserved cognitive function in old recipient mice, despite irradiation-induced suppression of neurogenesis, and without reducing ß2-microglobulin. Instead, young bone marrow transplantation preserved synaptic connections and reduced microglial activation in the hippocampus. Circulating CCL11 levels were lower in young bone marrow recipients, and CCL11 administration in young mice had the opposite effect, reducing synapses and increasing microglial activation. In conclusion, young blood or bone marrow may represent a future therapeutic strategy for neurodegenerative disease.

Acute postnatal exposure to brominated diphenylether 47 delays neuromotor ontogeny and alters motor activity in mice.

Polybrominated diphenyl ethers (PBDEs) are widely used commercial flame retardants that are accumulating in the environment. PBDEs may interfere with the development of key biological systems, thus leaving children vulnerable to functional impairments in adulthood. There is a growing literature of animal studies that show subtle changes in motor and cognitive function following acute or repeated perinatal exposure to PBDEs. 2,2',4,4'-Brominated diphenyl ether (BDE 47), a very stable PBDE congener, has been shown to accumulate in humans, perhaps as a breakdown product of other PBDEs. The current study examined developmental milestones in male C57BL/6 mice exposed to a single oral dose of BDE 47 (0, 1, 10, or 30 mg/kg) on postnatal day (PND) 10. Behavioral endpoints assessing sensory and motor maturation were examined on PNDs 12, 14, 16, 18, 32, and 88. Motor activity was also examined at 2 and 4 months in a separate group of mice. BDE 47 exposure (particularly the highest dose) significantly increased body weight on PND 47 and thereafter. There was altered ontogeny in a few measures of neuromotor development; however, other developmental milestones and sensory responses were not altered. Motor activity was altered at both 2 and 4 months, with BDE 47-treated mice (all dose groups) displaying pronounced hyperactivity at 4 months. These data indicate that acute exposure to BDE 47 during postnatal development may produce subtle changes in the development of neuromotor systems that may alter adult behavior.

Serum levels of tumour necrosis factor-alpha and interleukin-6 and their correlation with body mass index, weight loss, appetite and survival rate--preliminary data of Viennese outpatients with metastatic cancer during palliative chemotherapy.

The serum cytokine levels (in particular interleukine-6 (IL-6) and tumour necrosis factor-alpha (TNF-alpha)) of 61 advanced stage cancer patients receiving palliative chemotherapy as outpatients were determined with quantikine immunoassays. The values were correlated with body mass index (BMI), weight loss and appetite. Furthermore cytokine levels of patients who have died within one year were compared with those of patients who have survived more than a year. Serum levels of IL-6 (median: 1.93 pg/ml, range: 0.32-42.87) and of TNF-alpha (median: 2.55 pg/ml, range: 1.03-34.06) did not correlate with BMI, weight loss and appetite. Serum IL-6 levels of patients with survival time less than one year were significantly higher than the levels of patients who survived more than one year, no significant differences in TNF-alpha serum levels were evident. The data of this observation are consistent with current literature. Due to changes in serum levels of proinflammatory cytokines in response to chemotherapy and additional therapy, it is unlikely that IL-6 and TNF-alpha can be used as independent indicators for weight loss and appetite. Nevertheless, high serum levels of IL-6 correlate with short-time mortality.

Culture of subconfluent human fibroblasts and keratinocytes using biodegradable transfer membranes.

This study aims to assess the suitability of biodegradable membranes as transfer matrix materials for the culture of subconfluent fibroblasts and keratinocytes. The materials investigated were based on collagen, chitosan and enzyme-digestible cellulose. The proliferation and growth behaviour of human keratinocytes and dermal fibroblasts were analysed and morphology and distribution determined. Cultured fibroblasts exhibited no significant differences in proliferation for the different membrane types, whereas keratinocytes revealed significantly higher proliferation on collagen membranes compared with membranes based on cellulose and chitosan. Co-cultured fibroblasts and keratinocytes from the same donor on collagen membranes showed more homogenous cell distribution, but they segregated in heterologous co-cultures; this effect must be further investigated. Thus, collagen and collagen-coated chitosan membranes are suitable for the subconfluent transfer of human fibroblasts and keratinocytes.

Influence of dosing volume on the neurotoxicity of bifenthrin.

Pyrethroids are pesticides with high insecticidal activity and relatively low potency in mammals. The influence of dosing volume on the neurobehavioral syndrome following oral acute exposure to the Type-I pyrethroid insecticide bifenthrin in corn oil was evaluated in adult male Long Evans rats. We tested bifenthrin effects at 1 and 5 ml/kg, two commonly used dose volumes in toxicological studies. Two testing times (4 and 7 h) were used in motor activity and functional observational battery (FOB) assessments. Four to eight doses were examined at either dosing condition (up to 20 or 26 mg/kg, at 1 and 5 ml/kg, respectively). Acute oral bifenthrin exposure produced toxic signs typical of Type I pyrethroids, with dose-related increases in fine tremor, decreased motor activity and grip strength, and increased pawing, head shaking, click response, and body temperature. Bifenthrin effects on motor activity and pyrethroid-specific clinical signs were approximately 2-fold more potent at 1 ml/kg than 5 ml/kg. This difference was clearly evident at 4 h and slightly attenuated at 7 h post-dosing. Benchmark dose (BMD) modeling estimated similar 2-fold potency differences in motor activity and pyrethroid-specific FOB data. These findings demonstrate that dose volume, in studies using corn oil as the vehicle influences bifenthrin potency. Further, these data suggest that inconsistent estimates of pyrethroid potency between laboratories are at least partially due to differences in dosing volume.

Evaluation of developmental neurotoxicity of organotins via drinking water in rats: dimethyl tin.

Dimethyltin (DMT) is one of several organotins that are detected in domestic water supplies due to their use as plastic stabilizers for polyvinyl chloride (PVC) and chlorinated PVC (CPVC) products. A limited number of in vitro and in vivo studies suggest that DMT may produce developmental neurotoxicity; therefore, we initiated studies to evaluate long-term neurobehavioral changes in offspring following perinatal exposure. In the first study, female Sprague-Dawley rats were exposed via drinking water to DMT (0, 3, 15, 74 ppm) before mating and throughout gestation and lactation. Male offspring were tested for changes in: 1) preweaning learning in an associative runway task, 2) motor activity ontogeny, 3) spatial learning and retention in the Morris water maze as adults, 4) brain weight, 5) biochemical evidence of apoptosis, and 6) neuropathology. DMT toxicity was expressed as depressed maternal weight gain (74 ppm), and in the offspring, decreased brain weight (3, 74 ppm), decreased apoptosis (all concentrations), mild vacuolation in adult offspring (all concentrations), and slower learning in the water maze (15 ppm) due to altered spatial search patterns. In a second study, DMT exposure (same concentrations) occurred from gestational day 6 to weaning. Male and female offspring were tested. The high concentration again depressed maternal weight gain, decreased offspring birth weight and preweaning growth, and decreased brain weight. Increased and decreased apoptotic markers were measured, depending on age. Learning deficits were observed in the runway at postnatal day 11 (15, 74 ppm) and again in the adult offspring in the water maze (15 ppm). The results of both studies demonstrate a reproducible effect of 15 ppm perinatal DMT exposure on spatial learning. Changes in expression of apoptosis, brain weight, and the occurrence of neuropathological lesions also indicate potential neurotoxicity of DMT. These results were in contrast to earlier findings with monomethyl tin, for which only similar neuropathological lesions were observed. Thus, developmental neurotoxicity may be produced in offspring following gestational exposure to DMT in drinking water.

[Surgical treatment of high-voltage electrical injuries]. / Die chirurgische Behandlung von Hochspannungsverletzungen.

PURPOSE/BACKGROUND: High-voltage burns represent a challenging surgical entity. Compared to conventional burns, these injuries are characterized by an increased morbidity and worse potential for rehabilitation. The aim of the present study was to analyse the management of high-voltage injuries during the early posttraumatic period with special emphasis on the surgical procedures. PATIENTS/MATERIAL AND METHOD: We retrospectively evaluated the medical records of patients with electrical injuries treated from 1995 - 2007. A total of 61 patients (57 men, 4 females, mean age: 34 +/- 13 years) with high-voltage burns was included for analysis. RESULTS: The majority of high-voltage burns was work-related (75 %). The mean total burn area was 35 % of the total body surface, with a mean of 29 % deep burns. An average of 4.8 +/- 4 operations were performed per patient (range: 1 - 23 operations). Surgical procedures included repeated debridement/necrectomy (100 % of all patients), early escharotomy/fasciotomy (47.5 %), and amputations (18 %). 14 patients (23 %) underwent reconstructive surgery using either local or free flaps. The mortality rate was 15 %. CONCLUSION: The surgical management of high-voltage burns is characterised by repetitive debridements and necrectomies. Despite an aggressive approach to remove necrotic tissue, the mortality in this type of injury is considerably high. Limb salvage may be achieved with the use of free microvascular flaps. However, an amputation of necrotic extremities must be considered in the copresence of septic complications.