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Cyanotic congenital heart disease with decreased pulmonary blood flow in children.

Of the "five T's" of cyanotic congenital heart disease--tetralogy of Fallot, TGA, TAPVC, truncus, and tricuspid valve abnormalities (tricuspid atresia, stenosis, and displacement)--the first and last are commonly associated with diminished PBF. The four features that comprise tetralogy of Fallot--right ventricular hypertrophy, VSD, overriding aorta, and subpulmonary stenosis--are all secondary to a single morphogenetic defect: failure of expansion of the subpulmonary conus. This also explains the variability in clinical presentation. When neonates need intervention, shunts are usually performed. Coronary arterial anatomy must be defined before repair, which is usually done after these infants are 3 months of age. Although children with repaired tetralogy of Fallot are not completely "normal," markedly increased longevity and improvement in quality of life can be achieved. When major associated defects are present, such as atrioventricular canal defect, diminutive pulmonary arteries or collateral vessels, or left heart lesions, the prognosis changes from excellent to merely good. Tetralogy of Fallot with absent pulmonary valve syndrome is physiologically different from other tetralogy of Fallot conditions and characterized primarily by airway obstruction from massive dilatation of the central and perihilar pulmonary arteries; repair with pulmonary artery reduction is necessary. Tricuspid valve abnormalities include atresia, hypoplasia (i.e., pulmonary atresia with intact ventricular septum), and displacement (i.e., Ebstein anomaly). The pathophysiology that dictates these children's clinical condition (and prognosis) relates to three factors: (1) status of the tricuspid valve, (2) presence and size of a VSD, and (3) TGA or normally related great arteries. Virtually all children with tricuspid valve abnormalities can be palliated; reparative options include repair using two-ventricle, one-ventricle, or 1-1/2 ventricle repair. Children with critical pulmonary stenosis generally have a normal tricuspid valve and right ventricle. Balloon dilation is usually the only therapy necessary.

Algorithms↗

Dependency of location of salvageable myocardium on type of intervention.

The purpose of this study were (1) to determine the location of the salvageable border zone in relation to the ischemic coronary bed, and (2) to determine whether the location of salvaged tissue differs depending on the mechanism of salvage and the type of intervention. Forty-four open chest dogs were subjected to either 6 hours of occlusion of the left anterior descending coronary artery or 4 hours of occlusion of this artery followed by 2 hours of reperfusion. Dogs with 6 hours of occlusion received either saline solution (Group I, n = 9), ibuprofen, 12.5 mg/kg body weight, (Group II, n = 7), flurbiprofen, 1 mg/kg (Group III, n = 10), or L-hydroxyphenylglycine, 10 mg/kg (Group IV, n = 8) intravenously 30 minutes and 3 hours after coronary occlusion. Dogs in Group V (n = 10) were subjected to 4 hours of coronary occlusion followed by 2 hours of reperfusion, but received no drugs. Although from 17 to 42 percent of the myocardium at risk did not become infarcted in Groups II through V compared with only 6 percent in Group I, the location of salvaged tissue was different in dogs receiving reperfusion (Group V) from that of dogs receiving drug interactions (Groups II, III and IV). In Group V, the salvaged tissue was primarily subepicardial with virtually no lateral zone of salvaged tissue (ratio of salvaged subepicardium to salvaged subendocardium 14.8 +/- 1.9 to 1). In Groups II, III and IV, there was a portion of the myocardium at risk at both lateral margins that did not become infarcted, as well as a portion of subepicardial tissue (ratio of subepicardium to subendocardium salvaged 3.3 +/- 0.4 in Group II, 2.5 +/- 0.1 in Group III and 2.0 +/- 0.2 in Group IV). Thus, infarct size reduction by ibuprofen, flurbiprofen and L-hydroxyphenylglycine is accompanied by lateral and subepicardial zones of salvage, whereas tissue salvaged by reperfusion is located primarily in the subepicardium. These observations should help to resolve the controversy regarding the existence and location of the various zones of ischemic myocardium that can be salvaged by drugs or reperfusion.

Animals↗

Exercise-induced pulmonary hemorrhage.

EIPH is a condition affecting virtually all horses during intense exercise worldwide. The hemorrhage originates from the pulmonary vasculature and is distributed predominantly bilaterally in the dorsocaudal lung lobes. As the condition progresses, the lung abnormalities extend cranially along the dorsal portions of the lung. An inflammatory response occurs in association with the hemorrhage and may contribute to the chronic sequela. Although conflicting opinions exist as to its affect on performance, it is a syndrome that is thought to increase in severity with age. The most commonly performed method to diagnose EIPH at the present time is endoscopy of the upper airway alone or in combination with tracheal wash analysis for the presence of erythrocytes and hemosiderophages. Because horses may not bleed to the same extent every time and the bleeding may originate from slightly different locations, these diagnostic procedures may not be extremely sensitive or quantitative. At this time, there is no treatment that is considered a panacea, and the currently allowed treatments have not proven to be effective in preventing EIPH. Future directions for therapeutic intervention may need to include limiting inflammatory responses to blood remaining within the lungs after EIPH.

Animals↗

Integration of health care information systems.

Information is at the core of an effective response to virtually all of the new demands that health care institutions will face in the 1990s. New information that is differently organized, more timely, and more conveniently available will facilitate new interactions within the institution. The consistent theme of the new systems requirements introduced by CQI is tighter connection to the processes of patient care and integration of systems and data as those processes cross traditional organizational boundaries. Even the billing requirements are pushing in the same direction. Ironically, the dinosaurs descended from billing systems do not even perform very well as billing systems today, because payers want more clinical detail, in addition to information at very specific points during the patient-care process. This new management model changes our view of our systems. Instead of systems designed to create an after-the-fact record of patient care, we need to think in terms of systems that are part of the patient-care process. This is essential for the continuous monitoring and--when the process gets out of control--rapid intervention that are an intrinsic part of the process in the CQI model. Of course, these systems also produce a complete record as a by-product, but that is not their primary objective. These demands will test the capacities of many of our existing systems and will require the replacement of others. Like all complex processes, however, systems development is performed one step at a time. Each step is taken within the context of an overall goal but also presents an opportunity for learning. CQI is a new management model, and the system requirements are far from clear. Hence, we are likely to need a little continuous improvement in the systems, too.

Accounting↗

Juvenile arrest: a cross-cultural comparison.

BACKGROUND: Cross-national studies describing the psychopathological characteristics of arrested adolescents are virtually non-existent. Such studies are important because they have implications for national policy on arrest, case-management, and future research. METHOD: To address this issue, self-report surveys administered to representative groups of 12- to 16-year-old adolescents in New Haven, USA (N = 1138) and Antwerp, Belgium (N = 627) were compared. A number of internalizing and deviant behavior variables were compared between controls (C), non-arrested antisocial (NA), and arrested antisocial (AR) participants. RESULTS: Similar cross-national arrest rates and levels of antisocial behavior were found. NA and AR youths in both countries reported more internalizing problems, except for anxiety, and more deviant characteristics. Contrary to expectations, the level of depression was not higher in AR compared to NA youth when differences in antisocial behavior between NA and AR were controlled. Also unexpected, arrest showed an independent association with a number of deviant behavior variables. CONCLUSIONS: Further research should investigate the underlying mechanisms of these associations, as this insight would be useful for developing future intervention and prevention programs, as well as for developing future national policies regarding juvenile antisocial behavior.

Adolescent↗

Carotid endarterectomy in elderly patients: low complication rate with overnight stay.

HYPOTHESIS: Elderly patients undergoing carotid endarterectomy (CEA) can have a low complication rate and a short hospital stay. DESIGN: In this case series, we compared CEA results from January 1, 1994, through December 31, 1998, in 2 different age groups: 71 to 80 years and 81 years and older. SETTING: A private vascular surgery practice. PATIENTS: We studied 271 patients who underwent 293 CEAs; 124 procedures were for patients in the 71- to 80-year-old age group, and 42 procedures were for patients aged 81 years and older. INTERVENTIONS: Classic CEA was performed on all patients. From 1994 through 1996, 179 operations were performed under general anesthesia with routine shunting. In 1997 and 1998, 114 operations were performed under locoregional anesthesia with selective shunting. MAIN OUTCOME MEASURES: Length of hospital stay and 30-day morbidity and mortality. RESULTS: The mortality rate for the entire series was 0.7% (2 of 293 patients). Major cardiac complications occurred in 3 patients (1.0%). Perioperative stroke occurred in 3 cases(1.0%); 2 strokes occurred in patients aged 71 to 80 years (2 [1.6%] of 124 patients), and 1 occurred in a patient aged 81 years or older (1 [2.4%] of 42 patients). Two additional patients developed reversible ischemic neurological deficits but were not in the elderly group (> or =81 years and older). The mean hospital stay was 1.5 days for patients aged 71 to 80 years and 1.2 days for patients aged 81 years and older. All outcome variables were statistically similar in both age groups. CONCLUSION: Octogenarians can undergo CEA with little morbidity and mortality and virtually an overnight hospital stay.

Age Factors↗

[Eicosanoids and phospholipases].

Prostaglandins, thromboxanes, and leukotrienes have been implicated to play an important role in physiology as well as in a growing list of pathophysiologic conditions. These oxidation products of 8.11.14-eicosatrienoic-, 5.8.11.14.-eicosatetraenoic-, and 5.8.11.14.17.-pentaenoic acids have been collectively designated eicosanoids. Many clinically important diseases are associated with altered eicosanoid biosynthesis. Furthermore, a series of hormones are known to induce acutely formation of eicosanoids, suggesting a crucial role in a multitude of tissue responses including phenomena such as secretion, platelet aggregation, chemotaxis, and smooth muscle contraction. The major precursor for the eicosanoids seems to be 5.8.11.14.-eicosatetraenoic acid or arachidonic acid. Virtually all of arachidonic acid however is present in esterified form in complex glycerolipids. Since cyclooxygenase and the lipoxygenases utilize arachidonic acid in its free form, a set of acylhydrolases is required to liberate arachidonic acid from membrane lipids before eicosanoid formation can occur. It became only recently apparent that a minor acidic phospholipid, phosphatidylinositol, comprising only 5%-10% of the phospholipid mass in mammalian cells, plays an important role in arachidonic acid metabolism. Phosphatidylinositol--after phosphorylation to phosphatidylinositolphosphate and phosphatidylinositolbisphosphate--appears to be hydrolyzed by specific phospholipases C generating 1-stearoyl-2-arachidonoyl-diglyceride. Diglyceride serves as substrate for diglyceride lipase to form monoglyceride and free fatty acid. Alternatively diglyceride is phosphorylated by diglyceride kinase yielding phosphatidic acid, which is believed to be reincorporated into phosphatidylinositol. In addition to phosphatidylinositol phosphatidylcholine, phosphatidylethanolamine and phosphatidic acid may contribute to arachidonic acid release. These phospholipids are substrates for phospholipases A2 generating free arachidonic acid and the respective lysophospholipid. Understanding of the biochemistry of arachidonic acid liberation may be critical in developing strategies of pharmacological intervention in a variety of pathological conditions.

Animals↗

Biochemical dysfunction in heart mitochondria exposed to ischaemia and reperfusion.

Heart tissue is remarkably sensitive to oxygen deprivation. Although heart cells, like those of most tissues, rapidly adapt to anoxic conditions, relatively short periods of ischaemia and subsequent reperfusion lead to extensive tissue death during cardiac infarction. Heart tissue is not readily regenerated, and permanent heart damage is the result. Although mitochondria maintain normal heart function by providing virtually all of the heart's ATP, they are also implicated in the development of ischaemic damage. While mitochondria do provide some mechanisms that protect against ischaemic damage (such as an endogenous inhibitor of the F1Fo-ATPase and antioxidant enzymes), they also possess a range of elements that exacerbate it, including ROS (reactive oxygen species) generators, the mitochondrial permeability transition pore, and their ability to release apoptotic factors. This review considers the process of ischaemic damage from a mitochondrial viewpoint. It considers ischaemic changes in the inner membrane complexes I-V, and how this might affect formation of ROS and high-energy phosphate production/degradation. We discuss the contribution of various mitochondrial cation channels to ionic imbalances which seem to be a major cause of reperfusion injury. The different roles of the H+, Ca2+ and the various K+ channel transporters are considered, particularly the K+(ATP) (ATP-dependent K+) channels. A possible role for the mitochondrial permeability transition pore in ischaemic damage is assessed. Finally, we summarize the metabolic and pharmacological interventions that have been used to alleviate the effects of ischaemic injury, highlighting the value of these or related interventions in possible therapeutics.

Animals↗

Intravascular ultrasound assessment of direct percutaneous transluminal coronary angioplasty in patients with acute myocardial infarction.

BACKGROUND: Acute myocardial infarction is caused by sudden thrombotic occlusion of the coronary artery due to a previous rupture of atherosclerotic plaque. OBJECTIVE: To use intracoronary ultrasound measurements to evaluate lumen and plaque changes in patients with acute myocardial infarction. METHODS: Patients (n = 103) with acute myocardial infarction who had been scheduled to undergo primary percutaneous transluminal coronary angioplasty (PTCA) were selected. Both before and after successful coronary angioplasty, intracoronary 30 MHz ultrasound studies were performed using a 3.5F monorail catheter. The ultrasound catheter was successfully advanced into the occluded vessel segment without major complications prior to PTCA in 79 of 103 (76.7%) patients and after PTCA in 88 of 103 (85.3%) patients. RESULTS: The plaques were eccentric in 66 patients (83.5%). The plaque morphology was purely low echogenic in 14 (17.7%), highly echogenic in six (7.6%) and mixed in 59 (74.7%) patients. Partial (59 of 79, 74.7%) or ring-like calcification (3 of 79, 3.8%) was observed in 62 patients (78.5%). Plaque fissuring or dissection was detected prior to PTCA in 25 patients (31.7%). Coronary angioplasty successfully enlarged the inner luminal area from 2.1 +/- 0.7 to 7.4 +/- 1.9 mm2 (P < 0.01), whereas the plaque-thrombus area decreased significantly (13.8 +/- 1.7 mm2 before and 9.0 +/- 1.9 mm2 after PTCA; P < 0.01). The total vessel area remained virtually constant (15.9 +/- 1.9 mm2 before and 16.4 +/- 2.5 mm2 after PTCA, NS). PTCA-induced plaque rupture or dissection was observed in only 13 (16.5%) patients. CONCLUSION: Intracoronary ultrasound imaging can be performed safely and successfully prior and subsequent to PTCA in selected patients with acute myocardial infarction. Early reperfusion via PTCA seems to be attributable to a significant reduction in the amount of low-echogenic plaque and thrombus material, whereas factors like balloon-induced dissection and stretching of vessels play only a minor role.

Aged↗

Expression of Werner and Bloom syndrome genes is differentially regulated by in vitro HIV-1 infection of peripheral blood mononuclear cells.

In HIV infection, continuous immune activation leads to accelerated ageing of the adaptive immune system, similar to that observed in elderly people. We investigated the expression of WRN and BLM (genes involved in disorders characterized by premature ageing, genomic instability and cancer predisposition) in peripheral blood mononuclear cells (PBMC) activated in vitro with phytohaemagglutinin (PHA) and infected with different HIV-1 strains. The steady state levels of mRNA were analysed by reverse transcription-polymerase chain reaction (RT-PCR), and protein expression was assayed using immunocytochemistry and Western blot techniques. In uninfected PBMC, PHA stimulation induced an increase in BLM mRNA and protein expression, while WRN expression remained virtually unchanged. When PBMC were infected in vitro with a lymphotropic HIV-1 strain, the level of BLM mRNA showed a peak at 24 h of infection, followed by a decline to uninfected culture levels. A similar result failed to be seen using an R5-tropic HIV-1 strain. In accordance with mRNA expression, in HIV-infected cultures PBMC were stained more frequently and more intensely by a BLM-specific antibody as compared to uninfected cultures, staining peaking at 24. Conversely, WRN expression was not modulated by HIV-1. The proportion of cells showing BLM up-regulation, established by immunocytochemical staining, was much greater than the proportion of productively infected PBMC, as established by proviral DNA measurement. This result indicates that BLM up-regulation is probably a result of an indirect bystander cell effect. Activation of the BLM gene in infected PBMC suggests that premature ageing could be a further immunopathogenetic mechanism involved in HIV-induced immunodeficiency, and points to a possible new candidate target for innovative therapeutic intervention.

Adenosine Triphosphatases↗

Should hemoglobin be normalized in uremic patients?

Cardiovascular disease is virtually a sine qua non of chronic kidney disease, as is poor quality of life. Dialysis patient for example, have cardiovascular death rates 10 - 20 times those of the general population. Recent estimates indicate that at least half of all patients starting dialysis therapy will have an admission for a major cardiovascular event within 5 years, of which cardiac failure is the most common. Both experimental and clinical studies suggest that the cardiovascular system in uremia is in a state of premature senescence, one which is poorly suited to the supraphysiological hemodynamic demands to which it is subjected. Most patients develop cardiomyopathy, which clearly predisposes to cardiac decompensation. Anemia and hypertension are the most obvious modifiable overload parameters in uremic patients. Several prospective observational studies have demonstrated anemia to be an independent risk factor for each step in the process leading from hemodynamic overload, through maladpative left ventricular enlargement to left ventricular failure and death. This process starts with declining renal function, long before end-stage renal disease, the traditional time at which intervention has started to be seriously considered. The case for normal hemoglobin in patients with chronic kidney disease is still greatly disputed. Observational studies, which examine left ventricular size, quality of life, functional status, hospitalization and survival, are overwhelmingly supportive. Intervention trials, to date, suggest clear benefits of a physiological approach to anemia management in terms of quality of life, and likely benefits in terms of left ventricular stress minimisation and associated remodelling. Whether these translate into a reduction in outcomes like cardiac failure or death remains an unanswered question.

Anemia↗

Variability and reproducibility of arterial and venous circulation parameters in the forearm and calf measured at one-week intervals.

In 12 healthy men aged 22 to 29 years the variability of basal arterial blood flow, maximal arterial blood flow as induced by a 5-min arterial occlusion, vascular resistances, total venous capacity and venous emptying rate and the reproducibility of the measurements were studied in both the upper and lower limbs 3 times at one week's interval under strictly standardised conditions using an automatic venous occlusion plethysmograph. Means, medians, standard errors, and standard deviations were virtually identical or very similar without any statistically significant difference between the 3 study occasions; this implies that valid comparisons can be made when measurements are repeated at several days' interval provided measuring conditions are rigorously standardised. Basal and maximal arterial blood flows and venous emptying rates per 100 ml of tissue were significantly higher (p less than 0.05-p less than 0.001) in the forearm than in the calf. Variability of basal blood flow in terms of standard deviations and in terms of coefficients of variation computed from duplicate determinations were significantly higher than for the other parameters and significantly more elevated in the forearm than in the calf. Variability of maximal arterial blood flow and venous emptying rate also tended to be higher in the forearm than in the leg. The high variability and low reproducibility of basal arterial flow measurements are apparently due to a high degree of random biological variability in particular concerning the forearm vascular bed which makes the forearm basal blood flow poorly suitable for studying effects of interventions in cardiovascular control.

Adult↗

Long-term changes in corneal surface configuration after penetrating keratoplasty.

PURPOSE: To examine the long-term longitudinal changes in corneal surface configuration as determined by Fourier series harmonic analysis of videokeratography data and of visual acuity and refraction after penetrating keratoplasty (PK). DESIGN: Interventional case series. METHODS: One hundred thirty eyes of 130 consecutive patients who were scheduled for PK using 16 interrupted 10-0 nylon sutures were recruited. Spherical equivalent power, regular astigmatism component, irregular astigmatism (asymmetry and higher-order irregularity) component of the central cornea as determined by Fourier analysis of videokeragraphic data, spectacle-corrected visual acuity, and spherical equivalent were examined at 1 week, and at 1, 3, 6, 9, 12, 18, and 24 months after PK. RESULTS: Spherical equivalent power increased considerably for up to 1 month after PK, but thereafter showed no further appreciable change up to the final follow-up at 24 months. The regular astigmatism component decreased markedly for up to 6 months after PK, while the total irregular astigmatism (sum of the asymmetry and higher-order irregularity) component decreased considerably up to approximately 3 months, and then these showed no further relevant change for up to 24 months. Spectacle-corrected visual acuity also improved markedly until approximately 3 months after PK, after which it was virtually stable. Furthermore, important correlations were found between regular and irregular astigmatism and the spectacle-corrected visual acuity. CONCLUSIONS: Corneal surface configuration after PK appears to be stable by approximately 6 months after PK, concurrent with postkeratoplasty stabilization of visual acuity.

Adult↗

Metabolic syndrome.

The Metabolic syndrome is a widely prevalent and multi-factorial disorder. The syndrome has been given several names, including- the metabolic syndrome, the insulin resistance syndrome, the plurimetabolic syndrome, and the deadly quartet. With the formulation of NCEP/ATP III guidelines, some uniformity and standardization has occurred in the definition of metabolic syndrome and has been very useful for epidemiological purposes. The mechanisms underlying the metabolic syndrome are not fully known; however resistance to insulin stimulated glucose uptake seems to modify biochemical responses in a way that predisposes to metabolic risk factors. The clinical relevance of the metabolic syndrome is related to its role in the development of cardiovascular disease. Management of the metabolic syndrome involves patient-education and intervention at various levels. Weight reduction is one of the main stays of treatment. In this article we comprehensively discuss this syndrome- the epidemiology, pathogenesis, clinical relevance and management. The need to do a comprehensive review of this particular syndrome has arisen in view of the ever increasing incidence of this entity. Soon, metabolic syndrome will overtake cigarette smoking as the number one risk factor for heart disease among the US population. Hardly any issue of any primary care medical journal can be opened without encountering an article on type 2 diabetes, dyslipidemia or hypertension. It is rare to see type 2 diabetes, dyslipidemia, obesity or hypertension in isolation. Insulin resistance and resulting hyperinsulinemia have been implicated in the development of glucose intolerance (and progression to type 2 diabetes), hypertriglyceridemia, hypertension, polycystic ovary syndrome, hypercoagulability and vascular inflammation, as well as the eventual development of atherosclerotic cardiovascular disease manifested as myocardial infarction, stroke and myriad end organ diseases. Conversely, treatment and consequent improvement of insulin resistance have been shown to result in better outcomes in virtually all of these conditions.

Aspirin↗

Captopril protects against myocardial injury induced by magnesium deficiency.

We have previously reported that antioxidant drug intervention protects against magnesium deficiency-induced myocardial lesions. In the present study, Golden Syrian male hamsters were fed either a magnesium-deficient diet or a magnesium-supplemented diet. Animals from each group received sulfhydryl-containing angiotensin converting enzyme inhibitors: captopril, epi-captopril (a stereoisomer of captopril), and zofenopril* (arginine blend of zofenopril containing a free SH group); another group of animals received the non-sulfhydryl-containing angiotensin converting enzyme inhibitor enalaprilat. The animals were killed after 14 days, and their hearts were isolated for morphological and morphometric analyses. Hematoxylin and eosin-stained sections were examined by a computer image analysis system for a morphometric determination of the severity of myocardial injury. Captopril reduced both the density of lesions, from 0.32 to 0.08 lesions/(mm2) (p less than 0.01), and the area fraction of lesions, from 7.42 x 10(-4) to 2.03 x 10(-4) lesion area/(mm2) (p less than 0.01), as well as the degree of inflammatory infiltration around the blood vessels. Epi-captopril and zofenopril* were virtually equipotent to captopril, but enalaprilat afforded only slight (nonsignificant) protection. These results indicate that a significant component of the protective effect of captopril in this model was attributable to its sulfhydryl moiety, rather than solely due to the inhibition of the angiotensin converting enzyme. These data further support our previous findings of possible free radical participation in cardiomyopathy due to magnesium deficiency.

Analysis of Variance↗

Virtual exclusion and telework: barriers and opportunities of technocentric workplace accommodation policy.

Teleworking, a restructuring of the manner in which work occurs, based on information communication technologies (ICTs), is a promising way of further integrating people with disabilities into the workplace. In contrast to telecommuting, in which the work is primarily shifted in locale, telework is a restructuring of the tasks to be accomplished within the larger work setting which could result in "work" being done remotely, or collaboratively with coworkers (remotely or not) using ICTs. Drawing upon a review of the literature, this paper explores the relationship between telework and people with disabilities. While the advent of telecommuting and subsequently "teleworking" might open increased opportunities for the hiring of people with disabilities, it may also place severe constraints on the type of work, workplace environment and interactions, and accumulation of social capital for people with disabilities. Whereas much of the prevailing literature on telework and disability is often proscriptive in nature and is written with an audience of employers in mind, it is just as important to consider policy options from the standpoint of the employee as well. This paper proposes a number of policy approaches for the creation of an inclusive work environment for teleworkers with disabilities that can minimize, as much as possible, the social isolation faced by teleworkers with disabilities while maximizing their participation within the workplace community. Policy objectives for enhancing telework for people with disabilities fall into three general categories: 1) research, 2) outreach, and 3) interventions.

Persons with Disabilities↗

Computer assistance for intraoperative navigation in ENT surgery.

The intraoperative need for exact orientation during interventions in the paranasal sinuses and the augmented need for navigational aids in lateral skull base surgery have lead to the development of computer-aided tools during the last fifteen years. These tools, which provide the position of a tool or a pointer in the patient's preoperative radiologic imaging, have quickly gained a wide acceptance for revision surgeries and the surgical treatment of complex pathologies in Ear-, Nose- and Throat (ENT-) surgery. Currently, the use of such systems is spreading from academic centers to smaller hospitals and will become a standard tool in the near future. We review the present state of computer-aided surgery (CAS) systems, based on our experience as clinical and research centers with a long experience in the field, provide some technological background information and, based on selected cases, show the merits of this technology. The systems we have been working with cover a wide variety of intraoperative navigational systems in ENT surgery (Easy Guide, MedScan II, MKM, SNN, STN, SurgiGATE ORL, Treon, VectorVision, Viewing Wand, [without claiming completeness]), and virtually the whole area of ENT surgeries: macroscopic, (video-)endoscopic and microscopic procedures. The 3D tracking technologies involved cover mechanical, optical (active and passive), magnetic and robotic principles. The visualization tools used are computer monitors, video monitors, head-up-displays and the microscope's oculars, thus spanning the area from pointer-systems to real navigators and a surgical telepresence demonstrator, implementing the majority of available patient-to-image referencing strategies. Clinically, the systems can be operated with an acceptable accuracy of around 1 mm, whereas in laboratory settings and in cadaver studies application accuracy may be pushed to its limits: the physical resolution of the radiologic imaging used for navigation.

Journal Article↗

Assessment of effects of pinealectomy and exogenous melatonin administration on rat sciatic nerve suture repair: an electrophysiological, electron microscopic, and immunohistochemical study.

BACKGROUND: Collagen scar formation at the cut end of a nerve, an important problem in clinical practice for neurosurgeons in peripheral nerve surgery, obstructs sprouting of axons into appropriate distal fascicles, and thereby limits nerve regeneration. Researchers attempt to control collagen accumulation in the formation of neuroma by various physical and chemical methods, but these have yielded only limited functional success. This is the first experimental study investigating the effects of melatonin (MLT) on nerve repair and neuronal regeneration in rat sciatic nerve suture repair. METHODS: The hypothesis that exogenous MLT administration may inhibit the formation of neuroma in peripheral nerve surgery was investigated in rat sciatic nerve model. In this study, a total of 80 rats were used for control groups (Groups Ia, Ib, IIa, and IId), MLT group (Group Ic), surgical pinealectomy (Px) groups (Groups IIb and IIc), and group of MLT treatment following Px procedure (Group IIe). All animals underwent a surgical intervention consisting of bilateral sciatic nerve section and primary suture repair. At 8 weeks after repair, the animals were killed following completion of recording of nerve action potentials (NAPs). Then, unilateral sciatic nerve specimens including the suture repair region were carefully removed and the excised segments were processed for electron microscopy examination. Afterwards, contralateral sciatic nerve specimens from two animals from each group were removed and stained for immunohistochemical analysis. RESULTS: Results of morphometric analysis revealed that Px procedure caused an elevation of collagen content of the sciatic nerve and macroscopic neuroma formation, and that there was a statistically significant reduction in collagen content of the same region in pinealectomized animals treated with MLT (p<0.001). Accordingly, electrophysiological findings demonstrated that the stimulus intensities required to excite a NAP response were increased in surgical Px group, but the presence of a reduced threshold response was found in the group treated with MLT following Px procedure (p<0.01). Immunohistochemical staining for Type I collagen and Type III collagen was markedly more intense in the epineurium of animals after Px. Virtually no or only weak staining was observed in animals in control groups and the MLT treatment group. Results of immunohistochemical analysis revealed that surgical Px procedure caused a strong immunoreactivity for Type I collagen and Type III collagen in all connective tissue planes of the nerve, especially in the epineurium, and there was a statistically significant reduction in immunoreactivity of the repair region in animals receiving MLT treatment after Px procedure (p<0.001). CONCLUSION: This study demonstrates that exogenous MLT administration significantly inhibits collagen accumulation in the formation of neuroma in the suture repair site and thereby improves nerve regeneration. From a clinical standpoint, the positive effect of MLT administration on neuroma formation and nerve regeneration seems a particularly attractive treatment option. Therefore, we believe that nerve repair with addition of MLT may be a worthwhile option in addition to other treatment modalities in case of MLT deficiency, such as aging. However, further experimental and clinical studies using functional analysis warranted to confirm this result in future.

Action Potentials↗