abdelmo/pubmed-dataset · Datasets at Hugging Face

Crystallization and preliminary crystallographic study of triple-helical DNA.

conclusion that the sequences of the 12-mer and 9-mer oligonucleotides form a duplex DNA at one end and a triplex DNA at the other end.

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Optimization of the critical nuclear size for protein crystallization: a note.

It was observed that for some proteins the best crystals for X-ray diffraction have been obtained at supersaturation ratios of ca 2.5-3 (in experiments without seeding). It was then noticed that under certain conditions specific to the protein such values are close to a local minimum of the critical radius for nucleation. A relation between the two observations is proposed.

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Experiences and expectations of a novel X-ray microsource with focusing mirror. I. erratum

The following are corrections to a paper by Bloomer & Arndt [(1999); Acta Cryst. D55; 1672-1680]. The entry in the second row of the I(MAR) column of Table 1(b) on page 1674 should read 6.6 and not 16. 6. In Table 4 on page 1677 the source diameter should be given as 15 &mgr;m and not 15 mm; and the units for the diameter of the sample should be given as &mgr;m instead of mm.

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Notes for authors

nan

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Crystallization of helix pomatia agglutinin (HPA), a protein from the edible snail. erratum

One of the authors was omitted in the published version of the paper by Lisgarten et al. (1999) Acta Cryst. D55; 1903-1905. The full author list is given above.

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The role of human bone morphogenetic proteins in spinal fusion.

The attainment of a stable arthrodesis is critical to the successful management of some types of spinal disorders. Autologous iliac-crest bone graft has been the most commonly utilized substance associated with predictable healing in spinal fusion applications. Although alternative graft substances exist; these have not been shown to be as uniformly effective in achieving spinal fusion. Because of the morbidity associated with bone autograft harvest; there is increasing interest in alternative graft substan

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The role of human bone morphogenetic proteins in spinal fusion.

ces and especially in the osteoinductive abilities of bone morphogenetic proteins (BMPs). Several animal models have demonstrated that BMP-containing allograft or synthetic carrier medium is as effective as or superior to autograft bone in promoting spinal fusion. Furthermore; the limited number of human trials utilizing BMPs to treat nonunions in the appendicular skeleton indicate that the results found in animal models will be reproducible in the clinical setting.

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Orthopaedic aspects of child abuse.

Increased awareness of child abuse has led to better understanding of this complex problem. However; the annual incidence of abuse is estimated at 15 to 42 cases per 1;000 children and appears to be increasing. More than 1 million children each year are the victims of substantiated abuse or neglect; and more than 1;200 children die each year as a result of abuse. The diagnosis of child abuse is seldom easy to make and requires a careful consideration of sociobehavioral factors and clinical findings. Because

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Orthopaedic aspects of child abuse.

manifestations of physical abuse involve the entire child; a thorough history and a complete examination are essential. Fractures are the second most common presentation of physical abuse after skin lesions; and approximately one third of abused children will eventually be seen by an orthopaedic surgeon. Thus; it is essential that the orthopaedist have an understanding of the manifestations of physical abuse; to increase the likelihood of recognition and appropriate management. There is no pathognomonic fr

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Orthopaedic aspects of child abuse.

acture pattern in abuse. Rather; the age of the child; the overall injury pattern; the stated mechanism of injury; and pertinent psychosocial factors must all be considered in each case. Musculoskeletal injury patterns suggestive of nonaccidental injury include certain metaphyseal lesions in young children; multiple fractures in various stages of healing; posterior rib fractures; and long-bone fractures in children less than 2 years old. Skeletal surveys and bone scintigraphy with follow-up radiography may

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Orthopaedic aspects of child abuse.

be of benefit in cases of suspected abuse of younger children. The differential diagnosis of abuse includes other conditions that may cause fractures; such as true accidental injury; osteogenesis imperfecta; and metabolic bone disease. Management should be multidisciplinary; with the key being recognition; because abused children have a substantial risk of repeated abuse and death.

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Ballistics and gunshot wounds: effects on musculoskeletal tissues.

As a result of the increasing number of weapons in this country; as many as 500;000 missile wounds occur annually; resulting in 50;000 deaths; significant morbidity; and striking socioeconomic costs. Wounds are generally classified as low-velocity (less than 2;000 ft/sec) or high-velocity (more than 2;000 ft/sec). However; these terms can be misleading; more important than velocity is the efficiency of energy transfer; which is dependent on the physical characteristics of the projectile; as well as kinetic

10666650

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Ballistics and gunshot wounds: effects on musculoskeletal tissues.

energy; stability; entrance profile and path traveled through the body; and the biologic characteristics of the tissues injured. Although bullets are not sterilized on discharge; most low-velocity gunshot wounds can be safely treated nonoperatively with local wound care and outpatient management. Typically; associated fractures are treated according to accepted protocols for each area of injury. Treatment of low-velocity; low-energy fractures is generally dictated by the osseous injuries; as these are simil

10666650

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Ballistics and gunshot wounds: effects on musculoskeletal tissues.

ar in many regards to closed fractures. Soft tissues play a more critical role in high-velocity and shotgun fractures; which are essentially open injuries. Aside from perioperative prophylaxis; antibiotics are probably required only for grossly contaminated wounds; however; because contamination is not always apparent; most authors still recommend routine prophylaxis. High-energy injuries and grossly contaminated wounds mandate aggressive irrigation and debridement; including a thorough search for foreign m

10666650

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Ballistics and gunshot wounds: effects on musculoskeletal tissues.

aterial. Open fracture protocols including external fixation or intramedullary nailing and intravenous antibiotic therapy for 48 to 72 hours should be instituted. If there is vascular damage; exploration and repair are best performed after prompt fracture stabilization. Evaluation of the "four Cs"-color; consistency; contractility; and capacity to bleed-provides valuable information regarding the viability of muscle. Skin grafting is preferable when tension is required for wound closure; although other soft

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Ballistics and gunshot wounds: effects on musculoskeletal tissues.

-tissue procedures; such as use of local rotation flaps or free tissue transfer; may be necessary; especially for shotgun wounds. Distal neurologic deficit alone is not an indication for exploration; as it often resolves without surgical intervention.

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Arrhythmic risk stratification of post-myocardial infarction patients.

Post-myocardial infarction risk stratification; especially arrhythmic risk stratification; is an issue that has still not been wholly addressed in modern clinical cardiology. In the past 10 years; arrhythmic risk stratification has been approached mainly by evaluating frequency and complexity of premature ventricular contractions; detected on Holter monitoring; often in association with determination of percent ejection fraction. This methodology has been proven to be limited and fallacious according to the

10666655

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Arrhythmic risk stratification of post-myocardial infarction patients.

Cardiac Arrhythmia Suppression Trial I and II (CAST I;II) results; in which suppression of premature ventricular contractions or premature ventricular beats throughout by antiarrhythmic drugs resulted in an increase in both cardiac and arrhythmic mortality. Only amiodarone as an antiarrhythmic drug; as proven in the recent European Myocardial Infarct Amiodarone Trial (EMIAT) and Canadian Amiodarone Myocardial Infarction Trial (CAMIAT); was effective in reducing arrhythmic mortality without affecting cardia

10666655

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Arrhythmic risk stratification of post-myocardial infarction patients.

c mortality; in patients selected mainly because of a reduced ejection fraction; with and without premature ventricular contractions. Conversely; it is well known that beta-blockers are effective in preventing sudden death in post-acute myocardial infarction (AMI) patients; thus reducing cardiac and arrhythmic mortality. Conversely; in other institutions; risk stratification in post-AMI patients has been performed by electrophysiologic study obtained; without any previous noninvasive arrhythmic risk stratif

10666655

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Arrhythmic risk stratification of post-myocardial infarction patients.

ication; in all post-AMI patients. In recent years; many other noninvasive electrocardiology parameters; such as late potentials (signal-averaged electrocardiography); heart rate variability; baroreflex sensitivity; and; more recently; T-wave alternance; have been shown to be useful; but they are associated with a low specificity in the noninvasive identification of patients at high risk for arrhythmic mortality. Conversely; in the Multicenter Automatic Defibrillation Implantation Trial (MADIT); electrophys

10666655

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Arrhythmic risk stratification of post-myocardial infarction patients.

iology confirmed that inducibility of ventricular tachycardia shows high specificity and a high predictive value for arrhythmic events. Nevertheless; the MADIT study population is not comparable to a cohort of consecutive patients who have recently had a myocardial infarction. In this setting; the highest risk of arrhythmic events can be observed in patients with depressed percent ejection fraction (< 35%) and in the first 6 months after AMI. Today; the most convincing approach seems to be the one combining

10666655

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Arrhythmic risk stratification of post-myocardial infarction patients.

both noninvasive risk stratification parameters (e.g.; premature ventricular beats > 10/h or reduced heart rate variability < 70 ms or a positive signal-averaged electrocardiogram) followed by a further arrhythmic risk stratification; obtained through electrophysiologic study. Several published and ongoing trials that utilize various arrhythmic risk stratification techniques as part of their protocol are reviewed.

10666655

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Inpatient versus outpatient antiarrhythmic drug initiation: safety and cost-effectiveness issues.

Debate exists as to the proper site for initiating antiarrhythmic therapy for supraventricular tachyarrhythmias and other benign forms of ectopy: inpatient versus outpatient. Rapid detection of efficacy and adverse effects; with immediate correction of the latter; favors the inpatient site. Convenience and; under most circumstances; lower cost favor the outpatient site. Circumstances under which adverse event rates; including proarrhythmia; are expectedly low; would favor outpatient initiation. So would the

10666656

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Inpatient versus outpatient antiarrhythmic drug initiation: safety and cost-effectiveness issues.

use of an agent whose elimination half-life is so long as to render in-hospital monitoring to steady state highly impractical. Accordingly; outpatient initiation would be suitable for patients without structural heart disease receiving class IC drugs; patients with low risk for torsades de pointes receiving selected class III agents; in whom data in the literature are supportive (as has occurred with sotalol and azimilide); and patients who are to receive amiodarone. Transtelephonic electrocardiographic mo

10666656

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Inpatient versus outpatient antiarrhythmic drug initiation: safety and cost-effectiveness issues.

nitoring can be used to facilitate assessment in the outpatient setting. Inpatient initiation should be considered for patients with underlying sinus node or atrioventricular conduction disturbances; for patients with significant structural heart disease; for patients receiving a drug whose proarrhythmia may be idiosyncratic (e.g.; quinidine); and for patients who are to begin an antiarrhythmic drug while in a supraventricular tachyarrhythmia in whom sinus rhythm has not previously been seen. The relative c

10666656

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Inpatient versus outpatient antiarrhythmic drug initiation: safety and cost-effectiveness issues.

osts and benefits of the approach chosen will be a reflection of the probability that a drug with a chosen mechanism will cause an adverse outcome in a patient with a specific clinical substrate during the period chosen for monitoring.

10666656

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Aging successfully: the importance of physical activity in maintaining health and function.

Physicians caring for middle-aged and older patients frequently overlook the importance of regular physical activity. Exercise on a routine basis is an important component of successful aging. It has been shown that many age-related declines in musculoskeletal function can be markedly reduced by participation in some form of regular exercise. Examination of records from masters athletic competitions has been used to determine the true rate of age-related functional declines in highly trained; healthy indivi

10666651

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Aging successfully: the importance of physical activity in maintaining health and function.

duals and further supports these findings. Declines in physical abilities for masters athletes are gradual; which suggests that for many; the potential for participation in competitive athletics can persist well into the seventh decade of life. Recent studies indicate that health gains can be achieved with relatively low volumes of exercise. Indeed; the greatest benefit is seen when one "goes from doing nothing to doing something." Current data suggest that a cumulative total of 30 to 50 minutes of aerobic

10666651

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Aging successfully: the importance of physical activity in maintaining health and function.

exercise a day performed 3 to 5 days a week and one set of resistance exercises targeting the major muscle groups twice a week can produce significant health benefits. The aerobic conditioning requirement need not be a formal or structured activity; but can be satisfied through regular participation in many common physical tasks (e.g.; walking; gardening; housekeeping). Musculoskeletal injuries are a major cause of noncompliance with any exercise regimen and are especially debilitating for older individuals

10666651

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Aging successfully: the importance of physical activity in maintaining health and function.

. Prompt recognition of injury and treatment that emphasizes alternative conditioning exercises and minimizes "downtime" are especially important. Orthopaedists should be aware of the pattern of musculoskeletal injuries seen in this population; so as to assist their patients in avoiding these problems.

10666651

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Evaluation of chronic wrist pain.

Chronic wrist pain remains a challenge to diagnose and treat. A thorough history and physical examination are key. Various imaging techniques are essential to the evaluation of the patient with chronic wrist pain. Standard radiography; computed tomography; cinearthrography; magnetic resonance imaging; radionuclide imaging; arthroscopy; and arteriography all may have a role in assessment; and the orthopaedic surgeon should be familiar with the indications; strengths; and weaknesses of each. Laboratory tests

10666652

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Evaluation of chronic wrist pain.

may also be useful in evaluation. No all-inclusive algorithm can be applied in this setting; therefore; the physician must rely on his or her diagnostic acumen to successfully assess and treat chronic wrist pain.

10666652

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Molecular biology of arrhythmic syndromes.

In this review; the up-to-date understanding of the molecular basis of primary ventricular arrhythmias will be outlined. Two disorders have recently been well described at the molecular level; the long QT syndromes and Brugada syndrome; and in this paper we review the current scientific knowledge of each disease.

10666657

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Cost-effective strategies in the acute management of atrial fibrillation.

Atrial fibrillation is the most common sustained arrhythmia likely to be encountered in clinical practice. It is associated with significant morbidity and mortality. The treatment of patients with atrial fibrillation can be complex and costly; especially when patients are hospitalized for acute management of this arrhythmia. In this review; we summarize current approaches to the acute management of atrial fibrillation with an emphasis on the most cost-effective approaches. We review acute methods of heart r

10666658

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Cost-effective strategies in the acute management of atrial fibrillation.

ate control and cardioversion; including pharmacologic and other minimally invasive strategies. We believe that the most cost-effective approaches may require the use of standardized clinical pathways. This may help to ensure that patients with acute atrial fibrillation receive the most effective and efficient care.

10666658

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Surgical treatment of metastatic disease of the femur.

Nearly every malignant neoplasm has been described as having the capability to metastasize to bone. Of the estimated 1.2 million new cases of cancer diagnosed annually; more than 50% will eventually demonstrate skeletal metastasis. Advances in systemic and radiation therapy have led to a considerable improvement in the prognosis of patients with metastatic disease. As a result; orthopaedic surgeons are being asked with increasing frequency to evaluate and treat the manifestations of skeletal metastases. The

10666653

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Surgical treatment of metastatic disease of the femur.

femur is commonly the site of large impending lesions and complete pathologic fractures. Although the health status of some patients may preclude operative intervention; established pathologic fractures of the femur and metastatic lesions deemed likely to progress to imminent fracture generally should be treated surgically. A rational approach to selection of the proper treatment for these problems includes consideration of the patient's overall medical condition and the type; location; size; and extent of

10666653

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Surgical treatment of metastatic disease of the femur.

the tumor. Treatment principles are the same regardless of location. A construct should ideally provide enough stability to allow immediate full weight bearing with enough durability to last the patient's expected lifetime. All areas of weakened bone should be addressed at the time of surgery in anticipation of disease progression. To minimize disease progression and possible implant or internal fixation failure; postoperative external-beam irradiation should be considered.

10666653

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Catheter ablation in the year 2000.

After its introduction in 1987; radiofrequency catheter ablation became established as a safe and effective therapy for the cure of many cardiac arrhythmias in people. The possibility of assessing the relationship between the anatomical target and the electrophysiologic changes produced by radiofrequency pulse delivery has also provided significant improvement in the physician's knowledge of the pathophysiology of the underlying rhythm disturbance. Nowadays; using this therapy; success rates well above 90%

10666659

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Catheter ablation in the year 2000.

with recurrence rates lower than 5% are expected after treatment of most regular supraventricular arrhythmias. As catheter ablation techniques develop; success rates in the range of those obtained for regular supraventricular arrhythmias are expected in the future in the treatment of regular ventricular and irregular supraventricular arrhythmias.

10666659

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New advances in class III antiarrhythmic drug therapy.

In the past 2 years; significant advances have been made in class III antiarrhythmic drug therapy. In patients with ventricular arrhythmias and implantable cardioverter defibrillators (ICDs); antiarrhythmic agents are increasingly being used as adjunct therapy to decrease the frequency of ICD discharges. Sotalol was recently shown to be effective in reducing tachyarrhythmias in patients with ICDs. Intravenous amiodarone is being used for the acute treatment of unstable ventricular arrhythmia and is being in

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New advances in class III antiarrhythmic drug therapy.

vestigated for the treatment of acute out-of-hospital cardiac arrest. Class III agents are increasingly being used for prophylaxis in patients who have atrial fibrillation or atrial flutter; and data point to an important role for these agents in reducing supraventricular tachyarrhythmias after cardiac surgery. Future studies will need to directly compare these agents with pure anti-adrenergic maneuvers in postoperative patients. In addition to terminating atrial fibrillation and atrial flutter; ibutilide s

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New advances in class III antiarrhythmic drug therapy.

ignificantly reduces human atrial defibrillation thresholds and increases the percentage of patients who can be cardioverted from atrial fibrillation to sinus rhythm. The US Food and Drug Administration is expected to approve dofetilide for clinical use soon; and it is currently reviewing azimilide (which seems to be devoid of frequency-dependent effects on repolarization) for prophylaxis against atrial fibrillation and atrial flutter. Dronedarone; tedisamal; and trecetilide are now under active study inten

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New advances in class III antiarrhythmic drug therapy.

ded to determine their usefulness in patients with cardiac arrhythmias. Experimental studies are ongoing to identify pharmacologic agents that will selectively prolong repolarization in the atria without exerting electrophysiologic effects in the ventricles.

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Classification system of atrial fibrillation.

A number of publications and clinical trials on the management of atrial fibrillation (AF) deal with this arrhythmia as if it represents a single entity. As a result; advances made in recent years have not affected the way AF patients are treated in general practice except; perhaps; for the use of warfarin in anticoagulation. Therefore; there is a need for a classification system and for uniformity in the nomenclature used. The two terms currently used to describe AF; paroxysmal and chronic; require a time

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Classification system of atrial fibrillation.

frame. It is proposed that if an AF episode lasts longer than 7 days; the condition should be considered chronic. For the first symptomatic; non-self-terminating episode that is fewer than 7 days long; the term recent onset AF may be used; or recent discovery if the AF is asymptomatic or if the duration cannot be determined. Attacks of paroxysmal AF may differ in their duration; frequency; and functional tolerance. In the classification system described; three clinical aspects of paroxysmal AF were isolated

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Classification system of atrial fibrillation.

in such a way as to have implications for therapy. This classification system was found to be useful for characterizing different subsets of patients with AF.

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Amiodarone: clinical trials.

Amiodarone is an antiarrhythmic agent commonly used in the treatment of supraventricular and ventricular tachyarrhythmias. This article reviews the results and clinical implications of primary and secondary prevention trials in which amiodarone was used in one of the treatment arms. Key post-myocardial infarction primary prevention trials include the European Myocardial Infarct Amiodarone Trial (EMIAT) and the Canadian Amiodarone Myocardial Infarction Trial (CAMIAT); both of which demonstrated that amiodaro

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Amiodarone: clinical trials.

ne reduced arrhythmic but not overall mortality. In congestive heart failure patients; amiodarone was studied as a primary prevention strategy in two pivotal trials: Grupo de Estudio de la Sobrevida en la Insuficiencia Cardiac en Argentina (GESICA) and Amiodarone in Patients With Congestive Heart Failure and Asymptomatic Ventricular Arrhythmia (CHF-STAT). Amiodarone was associated with a neutral overall survival and a trend toward improved survival in nonischemic cardiomyopathy patients in CHF/STAT and impr

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Amiodarone: clinical trials.

oved survival in GESICA. In post-myocardial infarction patients with nonsustained ventricular tachycardia and a depressed ejection fraction; the Multicenter Automatic Defibrillator Implantation Trial (MADIT) demonstrated that implantable cardioverter-defibrillators (ICD) statistically improved survival compared to the antiarrhythmic drug arm; most of whose patients were taking amiodarone. In patients with histories of sustained ventricular tachycardia or ventricular fibrillation; the Cardiac Arrest Study in

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Amiodarone: clinical trials.

Seattle: Conventional Versus Amiodarone Drug Evaluation (CASCADE) trial demonstrated that empiric amiodarone lowered arrhythmic recurrence rates compared to other drugs guided by serial Holter or electrophysiologic studies. However; arrhythmic death rates were high in both treatment arms of the study. Several secondary prevention trials; including the Antiarrhythmics Versus Implantable Defibrillators Study (AVID); the Canadian Implantable Defibrillator Study (CIDS); and the Cardiac Arrest Study Hamburg (CA

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Amiodarone: clinical trials.

SH); have demonstrated the superiority of ICD therapy compared to empiric amiodarone in improving overall survival. Based on the above findings; amiodarone is safe to use in post-myocardial infarction and congestive heart failure patients that need antiarrhythmic therapy. Although amiodarone is effective in treating malignant arrhythmias; high-risk patients should be considered for an ICD as frontline therapy.

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Bibliography. Current world literature. Arrhythmias.

nan

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Clinical implication of antiembolic trials in atrial fibrillation and role of transesophageal echocardiography in atrial fibrillation.

Risk for stroke in patients with atrial fibrillation (AF) is highly heterogeneous. Increasing age; history of diabetes; hypertension; previous transient ischemic attack or stroke; and poor ventricular function are independent risk factors for stroke in patients with AF. Accordingly; some groups of patients with AF have low risk and some have high risk. In general; patients at high risk benefit most from anticoagulation therapy with warfarin. In general; if a patient is younger than 65 years of age and has n

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Clinical implication of antiembolic trials in atrial fibrillation and role of transesophageal echocardiography in atrial fibrillation.

one of the defined risk factors; the stroke rate without prophylaxis (aspirin or warfarin) is low. In patients 65 to 75 years of age with no risk factors; the risk for stroke is low with either aspirin or warfarin therapy; the choice is left to the caretaking physician. All patients older than 75 years and all patients of any age who have risk factors obtain striking benefit from the use of anticoagulation with warfarin. This benefit far outweighs any risk for major hemorrhage.

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Molecular abnormalities of the brain in Down syndrome: relevance to Alzheimer's neurodegeneration.

Down syndrome is caused by over-expression of genes located within a segment of chromosome 21; termed the Down locus. Down syndrome is associated with developmental abnormalities of the central nervous system that result in mental retardation and age-dependent Alzheimer-type neurodegeneration. Some of the neurodegenerative lesions; including A beta amyloid deposition; apoptotic cell death; and aberrant dendritic arborization; are in part due to constitutively increased expression of genes that encode the am

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Molecular abnormalities of the brain in Down syndrome: relevance to Alzheimer's neurodegeneration.

yloid precursor protein; superoxide dismutase I; and S100-beta; and located within the Down locus. However; neurodegeneration in Down syndrome is also associated with aberrant expression of genes that are not linked to the Down locus; including the growth associated protein; GAP-43; nitric oxide synthase 3; neuronal thread protein; and pro-apoptosis genes such as p53; Bax; and interleukin-1 beta-converting enzyme. Increased expression of these non-Down locus genes correlates with proliferation of dystrophic

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Molecular abnormalities of the brain in Down syndrome: relevance to Alzheimer's neurodegeneration.

neurites and apoptotic cell death; two important correlates of cognitive impairment in Alzheimer's disease. This article reviews the functional importance of abnormal gene expression in relation to Alzheimer-type neurodegeneration in brains of individuals with Down syndrome.

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Reduced aldehyde dehydrogenase levels in the brain of patients with Down syndrome.

Aldehyde dehydrogenase (ALDH) is a key enzyme in fructose; acetaldehyde and oxalate metabolism and represents a major detoxification system for reactive carbonyls and aldehydes. In the brain; ALDH exerts a major function in the metabolism of biogenic aldehydes; norepinephrine; dopamine and diamines and gamma-aminobutyric acid. Subtractive hybridization studies in Down Syndrome (DS) fetal brain showed that mRNA for ALDH are downregulated. Here we studied the protein levels in the brain of adult patients. The

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Reduced aldehyde dehydrogenase levels in the brain of patients with Down syndrome.

proteins from five brain regions of 9 aged patients with DS and 9 controls were analyzed by two-dimensional (2-D) gel electrophoresis and identified by matrix-assisted laser desorption ionization mass spectrometry. ALDH levels were reduced in the brain regions of at least half of the patients with Down Syndrome; as compared to controls. The decreased ALDH levels in the DS brain may result in accumulation of aldehydes which can lead to the formation of plaques and tangles reflecting abnormally cross-linked;

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Reduced aldehyde dehydrogenase levels in the brain of patients with Down syndrome.

insoluble and modified proteins; found in aged DS brain. Furthermore; we constructed a 2-Dmap including approximately 120 identified human brain proteins.

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The Down syndrome critical region.

Since the early 1970's numerous attempts have been made to learn whether specific segments of chromosome 21; when triplicated; are responsible for the clinical condition Down syndrome (DS). Studies were reported in which positive or negative clinical diagnoses of DS were made in the presence of partial trisomy of one or another segment of the chromosome. The distal half of the long arm of 21 (21q22) possesses most of the gene transcribing sites of the chromosome. It was this region that was thought to conta

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The Down syndrome critical region.

in loci essential to production of the clinical syndrome. Subsequent studies identified subregions of this band as "minimal" or "critical" sites necessary and sufficient to produce the clinical condition. A major problem with these assignments was that different investigators defined different critical/minimal regions. In 1994 evidence was presented in which regions of most of the long arm of chromosome 21 were said to contribute to the DS phenotype. Soon after; a report described a child with DS and partia

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The Down syndrome critical region.

l tetrasomy of the short arm and proximal long arm of 21; segments clearly distinct from the previously identified critical areas. Thus the clinical diagnosis of DS can be made in the presence of partial aneuploidy of nearly all segments of chromosome 21. It must be concluded that no evidence exists that individual loci on 21 are singularly responsible for specific phenotypic abnormalities in DS. Without exception; each of the clinical findings associated with DS is a multifactorial trait. The analysis of e

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The Down syndrome critical region.

ach trait in DS should thus be similar to analyses of the same traits in the general population with a focus on the way aneuploidy affects expression of multifactorial characteristics.

10666667

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Perioperative lower urinary tract infections and deep sepsis in patients undergoing total joint arthroplasty.

Deep sepsis in the involved joint after hip or knee arthroplasty may be the result of hematogenous seeding from a remote infectious source. This mechanism has been used to explain the well-documented association between postoperative urinary tract infections and subsequent joint infection after hip or knee arthroplasty. However; it is unclear whether there is an association between preoperative bacteriuria and deep prosthetic infection. The purpose of this review is to identify perioperative risk factors as

10666654

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Perioperative lower urinary tract infections and deep sepsis in patients undergoing total joint arthroplasty.

sociated with bacteriuria that have a positive correlation with deep joint sepsis following total hip or knee arthroplasty. The classic symptoms of dysuria; urgency; and frequency seen with urinary tract infections are often absent in the elderly despite the presence of urine coliforms; in these patients; pyuria (as indicated by the presence of more than 1x10(3) white blood cells per milliliter of noncentrifuged urine) may be used as a preliminary screening criterion. If there are irritative symptoms; the p

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Perioperative lower urinary tract infections and deep sepsis in patients undergoing total joint arthroplasty.

resence of more than 1x10(3) bacteria per milliliter of urine should be regarded as indicative of a urinary tract infection. If there is bacteriuria without symptoms of urinary irritation or obstruction; the current literature supports proceeding with total joint arthroplasty and treating those patients with urine colony counts greater than 1x10(3)/mL with an 8- to 10-day postoperative course of an appropriate oral antibiotic. Postponement of total joint surgery should be considered if preoperative evaluati

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Perioperative lower urinary tract infections and deep sepsis in patients undergoing total joint arthroplasty.

on reveals symptoms related to obstruction of the urinary pathway. Irritative symptoms in combination with a bacterial count greater than 1x10(3)/mL should also serve as an indication to postpone surgery. To diminish postoperative urinary tract infection; a bladder catheter should be inserted immediately preoperatively and removed within 24 hours of surgery to diminish the risk of urinary retention; which has been shown to increase the likelihood of a postoperative urinary tract infection.

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Neuropathology.

nan

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c-fos expression in brains of patients with Down syndrome.

c-fos is a protooncogene serving in multiple physiological processes in brain from signalling to proliferation and synaptic plasticity. We therefore decided to determine this transcription factor in control and Down Syndrome (DS) brain with the Rationale that c-fos may be linked to brain damage in DS. We determined mRNA steady state levels in frontal; parietal; occipital; temporal cortex and cerebellum of 9 patients with DS and 9 controls using RT-PCT. Significantly increased levels of mRNA c-fos normalized

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c-fos expression in brains of patients with Down syndrome.

versus the housekeeping gene beta-actin mRNA were found in frontal; parietal and temporal cortex of DS brain. c-fox mRNA levels comparable to controls were found in occipital cortex and cerebellum. Deteriorated c-fos expression in the individual brain regions may be linked to increased apoptosis and neurodegeneration; overexcitation by excitatory amino acids of reactive oxygen species.

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Neuronal cell death in Down's syndrome.

Down's syndrome (DS); occurring in 0.8 out of 1;000 live births; is a genetic disorder in which an extra portion of chromosome 21 leads to several abnormalities. With respect to the nervous system; it causes mental retardation. It is conceived that abnormal neuronal cell death in development is involved; but there is no direct evidence yet. In addition to developmental brain abnormalities; almost all DS brains over 40 years old manifest a similar pathology to Alzheimer's disease (AD); including the presence

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Neuronal cell death in Down's syndrome.

of senile plaques (SP) and neurofibrillary tangles (NFT). Although there was a debate to segregate dementia from underlying mental retardation; at least some portion of DS patients exhibit deteriorated mental status with aging. The mechanism underlying these abnormalities at the molecular level remains to be elucidated. Recently there have been several reports suggesting abnormalities reflecting increased risk to apoptosis in DS brains. Increased expression of several apoptosis-related genes (p53; fas; rat

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Neuronal cell death in Down's syndrome.

io of bax to bcl-2; GAPDH) in DS brains has been reported. Cultured neurons from both patients and model animals are reportedly more vulnerable to apoptosis. Overproduction of reactive oxygen species and its causative roles for increased apoptosis in DS tissues are suggested. One possible hypothesis is an increased susceptibility to apoptosis due to p53 overactivation in DS brains. A beta 42; a critical peptide for AD pathology from amyloid precursor protein (APP); can be detected in DS brains. A beta 42 is

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Neuronal cell death in Down's syndrome.

deposited in SP from an early stage; suggesting common molecular mechanisms in DS and AD. Animal models for DS are important in the search of molecular mechanisms. Several types of models are now available. Future DS studies are expected to integrate information from animal models and human tissues.

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Altered gene expression in fetal Down syndrome brain as revealed by the gene hunting technique of subtractive hybridization.

Information on gene expression in brain of patients with Down Syndrome (DS; trisomy 21) is limited and molecular biological research is focussing on mapping and sequencing chromosome 21. The information on gene expression in DS available follows the current concept of a gene dosage effect due to a third copy of chromosome 21 claiming overexpression of genes encoded on this chromosome. Based upon the availability of fetal brain and recent technology of gene hunting; we decided to use subtractive hybridizatio

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Altered gene expression in fetal Down syndrome brain as revealed by the gene hunting technique of subtractive hybridization.

n to evaluate differences in gene expression between DS and control brains. Subtractive hybridization was applied on two fetal brains with DS and two age and sex matched controls; 23rd week of gestation; and mRNA steady state levels were evaluated generating a subtractive library. Subtracted sequences were identified by gene bank and assigned by alignments to individual genes. We found a series of up- and downregulated sequences consisting of chromosomal transcripts; enzymes of intermediary metabolism; horm

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Altered gene expression in fetal Down syndrome brain as revealed by the gene hunting technique of subtractive hybridization.

ones; transporters/channels and transcription factors (TFs). We show that trisomy 21 or aneuploidy leads to the deterioration of gene expression and the derangement of transcripts describes the impairment of transport; carriers; channels; signaling; known metabolic and hormone imbalances. The dys-coordinated expression of transcription factors including homeobox genes; POU-domain TFs; helix-loop-helix-motifs; LIM domain containing TFs; leucine zippers; forkhead genes; maybe of pathophysiological significanc

10666671

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Altered gene expression in fetal Down syndrome brain as revealed by the gene hunting technique of subtractive hybridization.

e for abnormal brain development and wiring found in patients with DS. This is the first description of the concomitant expression of a large series of sequences indicating disruption of the concerted action of genes in this disorder.

10666671

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Gene expression in fetal Down syndrome brain as revealed by subtractive hybridization.

Information on gene expression in brain of patients with Down Syndrome (DS; trisomy 21) is limited and molecular biological research is focussing on mapping and sequencing chromosome 21. The information on gene expression in DS available follows the current concept of a gene dosage effect due to a third copy of chromosome 21 claiming overexpression of genes encoded on this chromosome. Based upon the availability of fetal brain and recent technology of gene hunting; we decided to use subtractive hybridizatio

10666672

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Gene expression in fetal Down syndrome brain as revealed by subtractive hybridization.

n to evaluate differences in gene expression between DS and control brains. Subtractive hybridization was applied on two fetal brains with DS and two age and sex matched controls; 23rd week of gestation; and mRNA steady state levels were evaluated generating a subtractive library. Subtracted sequences were identified by gene bank and assigned by alignments to individual genes. We found a series of up- and downregulated sequences consisting of chromosomal transcripts; enzymes of intermediary metabolism; horm

10666672

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Gene expression in fetal Down syndrome brain as revealed by subtractive hybridization.

ones; transporters/channels and transcription factors (TFs). We show that trisomy 21 or aneuploidy leads to the deterioration of gene expression and the derangement of transcripts described describes the involvement of chromosomes other than chromosome 21; explains impairment of transport; carriers; channels; signaling; known metabolic and hormones imbalances. The dys-coordinated expression of transcription factors including homeobox genes; POU-domain TFs; helix-loop-helix-motifs; LIM domain containing TFs;

10666672

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Gene expression in fetal Down syndrome brain as revealed by subtractive hybridization.

leucine zippers; forkhead genes; maybe of pathophysiological significance for abnormal brain development and wiring found in patients with DS. This is the first description of the concomitant expression of a large series of sequences indicating disruption of the concerted action of genes in that disorder.

10666672

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Molecular misreading of genes in Down syndrome as a model for the Alzheimer type of neurodegeneration.

The occurrence of +1 frameshifted proteins; such as amyloid precursor protein (APP+1) and ubiquitin-B (UBB+1) in Down syndrome (DS) has been linked to the onset of Alzheimer's disease (AD). In DS and AD patients; but also in elderly non-demented persons; these co-called +1 proteins accumulate in the neuropathological hallmarks (neurofibrillary tangles; dystrophic neurites of the neuritic plaques and neuropil threads) and may have deleterious effects on neuronal function. Frameshifts are caused by dinucleoti

10666673

[ null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null ]

Molecular misreading of genes in Down syndrome as a model for the Alzheimer type of neurodegeneration.

de deletions in GAGAG motifs in messenger RNA and are now thought to be the result of unfaithful transcription of normal DNA by a novel process termed "molecular misreading". In the present review some of the critical events in molecular misreading are discussed; the emphasis being on DS.

10666673

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Expression of the dihydropyrimidinase related protein 2 (DRP-2) in Down syndrome and Alzheimer's disease brain is downregulated at the mRNA and dysregulated at the protein level.

Deteriorated migration; axonal pathfinding and wiring of the brain is a main neuropathological feature of Down Syndrome (DS). Information on the underlying mechanisms is still limited; although basic functions of a series of growth factors; cell adhesion molecules; guidance factors and chemoattractants for brain histogenesis have been reported. We used proteomics to detect differences in protein expression between control; DS and Alzheimer's disease brains: In five individual brain regions of 9 individuals

10666674

[ null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null ]

Expression of the dihydropyrimidinase related protein 2 (DRP-2) in Down syndrome and Alzheimer's disease brain is downregulated at the mRNA and dysregulated at the protein level.

of each group we performed two dimensional electrophoresis with MALDI--identification of proteins and determined mRNA levels of DRP-2. Significantly decreased mRNA levels of DRP-2 in four brain regions of patients with DS but not with AD as compared to controls were detected. 2D electrophoresis revealed variable expression of DRP-2 proteins; which showed a high heterogeneity per se. Dysregulation of DRP-2 was found in brains of patients with DS and AD presenting with an inconsistent pattern; which in turn m

10666674

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Expression of the dihydropyrimidinase related protein 2 (DRP-2) in Down syndrome and Alzheimer's disease brain is downregulated at the mRNA and dysregulated at the protein level.

ay reflect the inconsistent neuropathological findings in patients with DS and AD. The decrease of mRNA DRP-2 steady state levels in DS along with deteriorated protein expression of this repulsive guidance molecule of the semaphorin/collapsin family; may help to explain deranged migration and histogenesis of DS brain and wiring of AD brain.

10666674

[ null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null, null ]

Gene expression relevant to Down syndrome: problems and approaches.

The long arm of human chromosome 21 likely contains several hundred genes. To determine which of these are responsible for specific aspects of the Down Syndrome phenotype; protein functional analysis coupled to phenotypic analysis of transgenic mice will be required. Because such experiments are both time consuming and expensive; prioritizing 21q genes for further studies would be advantageous. Here; we discuss expression analysis; specifically the use of Northern analysis; cDNA array screening and RNA tiss

10666675

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Gene expression relevant to Down syndrome: problems and approaches.

ue in situ hybridization to assess place and time of expression of forty-two genes. For a subset of these; over expression in normal versus trisomy cell lines and mouse tissues is discussed. Lastly; several examples of alternative processing and their potential for generation of brain specific proteins are described. Together; these experiments give information on time; place and level of expression of a number of 21q genes and suggest some interesting candidates worth further investigation for relevance to

10666675

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Gene expression relevant to Down syndrome: problems and approaches.

Down Syndrome. These data also illustrate the complexities and ambiguities inherent in interpretation and use of expression information.

10666675

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Isolation and analysis of chromosome 21 genes potentially involved in Down syndrome.

nan

10666676

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Differential display reveals deteriorated mRNA levels of NADH3 (complex I) in cerebellum of patients with Down syndrome.

Although gene hunting has been carried out in Down Syndrome (DS) cells; information on expressional differences in DS brain is limited. We have recently described expressional differences in fetal DS brain but cannot assign these findings to "DS per" se or simply to "neurodegeneration". We therefore performed gene hunting in cerebellum of adult patients with DS and Alzheimer's disease (AD) neuropathology; AD and controls. The gene hunting method used was differential display and pools of the individual grou

10666677

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Differential display reveals deteriorated mRNA levels of NADH3 (complex I) in cerebellum of patients with Down syndrome.

ps were examined to rule out allelic differences. Differential display revealed the absence of a band; identified by sequencing and gene bank work as matching the NADH3 gene (99.1% identity) in cerebellum of DS patients. Dot blots showed the presence of NADH3 signals in only two out of 7 DS patients. We show at the transcriptional level that a mitochondrial enzyme; the complex I; NADH3; is significantly downregulated in DS cerebellum. This extends previous work on deficiencies of the electron transport chai

10666677

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Differential display reveals deteriorated mRNA levels of NADH3 (complex I) in cerebellum of patients with Down syndrome.

n in platelets of patients with DS.

10666677

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Serotonin (5-HT) in brains of adult patients with Down syndrome.

Down syndrome (DS) is a genetic disease with developmental brain abnormalities resulting in early mental retardation and precocious; age dependent Alzheimer-type neurodegeneration. Furthermore; non-cognitive symptoms may be a cardinal feature of functional decline in adults with DS. As the serotonergic system plays a well known role in integrating emotion; cognition and motor function; serotonin (5-HT) and its main metabolite; 5-hydroxyindol-3-acetic acid (5-HIAA) were investigated in post-mortem tissue sam

10666678

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Serotonin (5-HT) in brains of adult patients with Down syndrome.

ples from temporal cortex; thalamus; caudate nucleus; occipital cortex and cerebellum of adult patients with DS; Alzheimer's disease (AD) and controls by use of high performance liquid chromatography (HPLC). In DS; 5-HT was found to be age-dependent significantly decreased in caudate nucleus by 60% (DS: mean +/- SD 58.6 +/- 28.2 vs. Co: 151.7 +/- 58.4 pmol/g wet tissue weight) and in temporal cortex by about 40% (196.8 +/- 108.5 vs. 352.5 +/- 183.0 pmol/g); insignificantly reduced in the thalamus; comparabl

10666678

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Serotonin (5-HT) in brains of adult patients with Down syndrome.

e to controls in cerebellum; whereas occipital cortex showed increased levels (204.5 +/- 138.0 vs. 82.1 +/- 39.1 pmol/g). In all regions of DS samples; alterations of 5-HT were paralleled by levels of 5-HIAA; reaching significance compared to controls in thalamus and caudate nucleus. In AD; 5-HT was insignificantly reduced in temporal cortex and thalamus; unchanged in cerebellum; but significantly elevated in caudate nucleus (414.3 +/- 273.7 vs. 151.7 +/- 58.4 pmol/g) and occipital cortex (146.5 +/- 76.1 vs

10666678

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Serotonin (5-HT) in brains of adult patients with Down syndrome.

. 82.1 +/- 39.1 pmol/g). The results of this study confirm and extend putatively specific 5-HT dysfunction in basal ganglia (caudate nucleus) of adult DS; which is not present in AD. These findings may be relevant to the pathogenesis and treatment of cognitive and non-cognitive (behavioral) features in DS.

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