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Recurrent Attacks (recurrent + attack)

Distribution by Scientific Domains

Medical Sciences	80%

Selected Abstracts

Biofilm formation and changes in bacterial cell surface hydrophobicity during growth in a CAPD model system

JOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 7 2004
G. W. Hanlon
Peritonitis is a frequent complication of continuous ambulatory peritoneal dialysis (CAPD), with patients suffering recurrent attacks. The microorganisms most frequently implicated in the infection are the skin microflora, in particular, the coagulase-negative staphylococci such as Staphylococcus epidermidis. These microorganisms gain access to the peritoneal cavity via the in-dwelling silicone rubber catheter in the abdominal wall and often persist as biofilms on the surface of the catheter. The surface characteristics of S. epidermidis were monitored during growth in a CAPD in-vitro model together with their ability to adhere to silicone rubber substrata. Fresh dialysis fluid exerted an injurious effect on the cells leading to a decrease in cell numbers but during the simulated dialysis period the cells adapted to the applied stresses. Over a 96-h period in the model both a clinical isolate and a skin isolate of S. epidermidis adopted a more hydrophobic phenotype. The data presented here show that the bacteria grown in this in-vivo reflective CAPD model continually adapt to their environment and become more tolerant to the stresses imposed. The adapted cells were seen to colonise silicone rubber substrata. [source]

Potassium channel blocker 4-aminopyridine is effective in interictal cerebellar symptoms in episodic ataxia type 2 , A video case report

MOVEMENT DISORDERS, Issue 9 2008
Matthias Löhle MD
Abstract Episodic ataxia type 2 (EA2) is an autosomal-dominant hereditary disorder clinically characterized by recurrent attacks of vertigo, imbalance and ataxia. Studies have shown that 4-aminopyridine (4-AP) is capable to prevent these attacks. However, there are no reports whether 4-AP is able to attenuate interictal cerebellar ataxia. Using the scale for assessment and rating of ataxia (SARA), we examined the efficacy of 4-AP on interictal ataxia in a 63-year-old female patient who suffered from EA2 since the age of 57. EA2 was diagnosed based on clinical criteria and not genetically proven. When treatment with 4-AP was paused the patient was suffering from marked gait and stance ataxia. After re-initiation of treatment with 5 mg 4-AP t.i.d., there was pronounced improvement in gait and stance ataxia. Within 24 hours SARA score lowered from 8.5 to 4.5 points. We conclude that 4-AP may be beneficial for interictal cerebellar ataxia in late onset EA2. © 2008 Movement Disorder Society [source]

Myoclonic status epilepticus: Video presentation,,

MOVEMENT DISORDERS, Issue 2 2002
Aman Badhwar BSc
A young woman with juvenile myoclonic epilepsy had recurrent attacks of myoclonic status epilepticus related to a long history of limited compliance and irregular sleep. The diagnosis of this clinical pattern is based mainly on clinical description. A home video captured an attack. © 2002 Movement Disorder Society. [source]

Disorders of carnitine transport and the carnitine cycle,

AMERICAN JOURNAL OF MEDICAL GENETICS, Issue 2 2006
Nicola Longo
Abstract Carnitine plays an essential role in the transfer of long-chain fatty acids across the inner mitochondrial membrane. This transfer requires enzymes and transporters that accumulate carnitine within the cell (OCTN2 carnitine transporter), conjugate it with long chain fatty acids (carnitine palmitoyl transferase 1, CPT1), transfer the acylcarnitine across the inner plasma membrane (carnitine-acylcarnitine translocase, CACT), and conjugate the fatty acid back to Coenzyme A for subsequent beta oxidation (carnitine palmitoyl transferase 2, CPT2). Deficiency of the OCTN2 carnitine transporter causes primary carnitine deficiency, characterized by increased losses of carnitine in the urine and decreased carnitine accumulation in tissues. Patients can present with hypoketotic hypoglycemia and hepatic encephalopathy, or with skeletal and cardiac myopathy. This disease responds to carnitine supplementation. Defects in the liver isoform of CPT1 present with recurrent attacks of fasting hypoketotic hypoglycemia. The heart and the muscle, which express a genetically distinct form of CPT1, are usually unaffected. These patients can have elevated levels of plasma carnitine. CACT deficiency presents in most cases in the neonatal period with hypoglycemia, hyperammonemia, and cardiomyopathy with arrhythmia leading to cardiac arrest. Plasma carnitine levels are extremely low. Deficiency of CPT2 present more frequently in adults with rhabdomyolysis triggered by prolonged exercise. More severe variants of CPT2 deficiency present in the neonatal period similarly to CACT deficiency associated or not with multiple congenital anomalies. Treatment for deficiency of CPT1, CPT2, and CACT consists in a low-fat diet supplemented with medium chain triglycerides that can be metabolized by mitochondria independently from carnitine, carnitine supplements, and avoidance of fasting and sustained exercise. © 2006 Wiley-Liss, Inc. [source]

4252: An introduction to autoinflammatory syndromes

ACTA OPHTHALMOLOGICA, Issue 2010
B BODAGHI
To define the spectrum and pathophysiology of autoinflammatory syndromes. This term has been proposed to describe a new group of diseases characterized by attacks of seemingly unprovoked inflammation in the absence of pathogens, without significant levels of autoantibodies and autoreactive T cells. Hereditary periodic fever syndrome, Crohn's disease, Blau syndrome, Chronic infantile neurologic cutaneous and articular syndrome and Muckle-Wells syndrome are examples of autoinflammatory conditions characterized by recurrent attacks of inflammation without any association with auto-antigens. The study of autoinflammatory diseases has progressed from genetics to definition of the functional defects. Although a direct association between defective innate immune responses to bacterial components and these diseases has not been established yet, this hypothesis remains highly plausible. Mutations in genes encoding the tumour necrosis factor (TNF) receptor and pyrin superfamilies of molecules may induce persistence of leukocytes that would ordinarily undergo apoptosis with further amplification of inflammatory stimuli. The use of biologics may control some of these conditions. [source]