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Biomedical subjects

M Levin

Publications and source records attributed to M Levin.

At least 55 records · Page 3Linked to original sources
PubMed2000

Personality in adolescents with chronic fatigue syndrome.

Our aim was to study the presence of personality traits and disorder in adolescents with Chronic Fatigue Syndrome (CFS). Personality was then compared to other measures of functioning such as presence of psychiatric disorder and rating on the Child Behavior Checklist 4-18 (CBCL) and in relation to CFS outcome. Twenty-five adolescents with CFS followed-up after contacts with tertiary paediatric/psychiatric clinics were compared with 15 matched healthy controls. Interviews and questionnaires from parents and youngsters included Personality Assessment Schedule (PAS), Kiddie-SADS Psychiatric Interview, Child Behavior Checklist. CFS subjects were significantly more likely than controls to have personality difficulty or disorder. Personality features significantly more common amongst them were conscientiousness, vulnerability, worthlessness and emotional lability. There was a nonsignificant association between personality disorder and worse CFS outcome. Personality difficulty or disorder was significantly associated with psychological symptoms and decreased social competence on the CBCL but it was distinguishable from episodic psychiatric disorder. Personality difficulty and disorder are increased in adolescents with a history of CFS. Personality disorder may be linked to poor CFS outcome.

Adolescent↗
PubMed2000

Inherited predisposition to mycobacterial infection: historical considerations.

Although one third of the world's population is estimated to be infected with Mycobacterium tuberculosis, only one tenth of infected individuals develop clinical disease. There is substantial epidemiological evidence that host genetic factors are important determinants of susceptibility to mycobacterial disease. This paper gives a historical context to the recent exciting advances in the field which have led to the identification of a number of human mycobacterial susceptibility genes.

Animals↗
PubMed2000

Ultrastructure of the horse tongue: further observations on the lingual integumentary architecture.

This investigation examined primarily epidermal specializations of the adult horse tongue by light, scanning and transmission electron microscopy. Samples were collected from seven regions of the normal tongue of various breeds of horse. The filiform papillae, present on the dorsal and lateral aspects but not the ventral aspect of the tongue, were short, slender and finger-like structures with variable-shaped terminae. The epidermal thickness and height of dermal ridges were reduced on fungiform and vallate papillae, but tissue architecture and keratinocyte ultrastructure of most of the lingual epidermis corresponded to the common mammalian epidermal paradigm. One unique finding was the highly localized clustering of epidermal cells with exceptionally high content of PAS-negative trichohyalin cytoplasmic granules at a location atop the dermal ridges and beneath the base of filiform papillae. These granular cells were immediately subjacent to clusters of clear, non-granulated epidermal cells. It is believed that this integumentary specialization may enhance the structural strength at this localized site of the tissue architecture, in relationship to the mechanical papillae.

Animals↗
PubMed2000

Pedunculated malignant melanoma.

BACKGROUND: The pedunculated melanoma is an unusual variant of nodular melanoma that presents a challenge in staging and management. OBJECTIVE: We discuss the clinical and histopathologic characteristics of a case of pedunculated melanoma and present a brief review of the literature. METHODS: Routine stain with hematoxylin and eosin was performed on tissue specimens. RESULTS: The pedunculated melanoma was excised. Sentinel lymph node dissection was performed and was negative for the presence of melanoma. CONCLUSIONS: Pedunculated melanoma is a rare type of melanoma. Conventional staging methods for melanoma may not be reliable in this type of tumor. Complete workup, possibly including sentinel lymph node dissection, should be performed in all patients with pedunculated melanomas.

Adult↗
PubMed2000

Case reports: headache caused by a spinal cord stimulator in the upper cervical spine.

We report persistent headaches developing in a patient subsequent to the placement of a spinal cord stimulator in the upper cervical spine. These persistent headaches responded to dihydroergotamine and sumatriptan. Headaches ceased upon repositioning of the stimulator lower in the cervical spine. We postulate an effect of the device on the trigeminovascular system via the nucleus caudalis trigeminalis and/or spinal trigeminal tract.

Brachial Plexus Neuritis↗
PubMed2000

Disseminated intravascular coagulation and purpura fulminans secondary to infection.

Infection is one of the commonest causes of disseminated intravascular coagulation (DIC). DIC is a complex disorder that results from an imbalance of the pro- and anticoagulant regulatory pathways. This chapter will explain the cellular and molecular basis of the disorder and consider the rationale behind current and experimental treatment strategies.

Bacterial Infections↗
PubMed2000

Jewish bioethics?

"Jewish Bioethics" as currently formulated has been criticized as being of parochial concern, drawing on obscure methodology, employing an authoritarian (and, to the modern mind, unintelligible) method of discourse and as being of little relevance to the wider community. We analyze Jewish bioethics in terms of rule and principle theory and demonstrate that it is based on rational consideration and reproducible reasoning. This approach allows methodological and terminological translation into a Western method of discourse that, in turn, has much to contribute to clarifying underlying principles and methods of application of modern bioethics.

Ethics, Medical↗
PubMed2000

A myocardial cytotoxic process is involved in the cardiac dysfunction of meningococcal septic shock.

OBJECTIVE: Myocardial dysfunction is a characteristic component of meningococcal septic shock and contributes to the persisting high mortality from the disease. Specific treatment of the myocardial failure has been hampered by the lack of understanding of its pathophysiology. We were interested to determine whether myocardial cell death was occurring in the presence of meningococcal septicemia and whether it correlated with the degree of left ventricular dysfunction and disease severity. We therefore investigated the release of cardiac troponin I (cTnI), a sensitive and specific marker of myocardial cell death, and related this to the severity of disease and cardiac dysfunction. DESIGN: Prospective study SETTING: Pediatric intensive care unit SUBJECTS: Patients admitted to the pediatric intensive care unit with a diagnosis of meningococcal septicemia. INTERVENTIONS: Serum concentrations of cTnI were determined at admission to intensive care in 101 children with meningococcal septicemia and serially in 37 children. Changes in cTnI were related to disease severity as measured by the Pediatric Risk of Mortality score and two markers of cardiac dysfunction. MEASUREMENTS AND MAIN RESULTS: Serum concentrations of cTnI were elevated above the range for healthy children in 24% of children with meningococcal septicemia at admission and in 62% of patients within 48 hrs. The peak concentrations occurred between 12 and 36 hrs after admission. There were significant correlations between cTnI levels and disease severity and between cTnI levels and the degree of myocardial depression measured by quantitative transthoracic echocardiography and peak inotrope requirements. CONCLUSIONS: The elevated serum concentrations of cTnI indicate that myocardial cell death is occurring in meningococcal septicemia. The relationship between cTnI and markers of myocardial function suggest that the cell death may have a role in the pathogenesis of myocardial dysfunction in meningococcal septicemia. Elucidation of the mechanism responsible for myocardial injury may lead to the development of therapeutic interventions to prevent or limit this cardiac damage.

Adolescent↗
PubMed2000

Increased excretion of urinary glycosaminoglycans in meningococcal septicemia and their relationship to proteinuria.

OBJECTIVES: Meningococcal septic shock is a devastating illness associated with an increase in vascular permeability leading to hypovolemia and accumulation of plasma proteins and fluid in tissues. The capillary leak syndrome is often associated with widespread thrombosis in the skin, limbs, and digits. We postulated that the increase in vascular permeability and the intravascular thrombosis might be caused by an inflammation-induced loss of endothelial and basement membrane glycosaminoglycans (GAGs), which play a role in the permeability and thromboresistant properties of the microvasculature. DESIGN: Prospective, single-center observational study. SETTING: University-affiliated meningococcal research unit and pediatric intensive care unit. PATIENTS: Eighteen children requiring intensive care for meningococcal sepsis, 18 children with steroid-responsive nephrotic syndrome, and 18 healthy control children. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Serum concentrations and urine excretion of glycosaminoglycans were measured and related to changes in glomerular permeability to plasma proteins. The size-distribution and nature of glycosaminoglycans were defined by Polyacrylamide Gel Electrophoresis and specific enzyme digestion. Urinary excretion of heparan sulfate, chondroitin-4-sulfate, and chondroitin-6-sulfate were significantly increased in meningococcal disease (MD) relative to healthy controls and children with steroid-responsive nephrotic syndrome. The urinary GAGs in MD were of similar size to those in controls when analyzed after pronase digestion. However, analysis of proteoglycan size before proteolytic digestion showed the urinary GAGs in MD were of lower molecular weight and unattached to proteins. The fractional excretion of albumin and immunoglobulin G in MD increased with severity of disease. Patients with severe or fatal MD had albumin clearances overlapping those seen in steroid-responsive nephrotic syndrome. There was a significant correlation between proteinuria in MD and urinary excretion of heparan sulfate (r2 = 0.611, p < .0001), chondroitin-4-sulfate (r2 = 0.721, p < .0001), and chondroitin-6-sulfate (r2 = 0.395, p < .0001). CONCLUSIONS: The capillary leak in meningococcal disease is associated with increased plasma and urine concentrations of GAGs, which may be proteolytically cleaved from endothelial and basement membrane sites. The correlation between the severity of protein leakage and the urine excretion of GAGs suggests that loss of GAGs may be causally related to the increase in permeability to proteins.

Child↗
PubMed2000

Intimal hyperplasia recurs after removal of PDGF-AB and -BB inhibition in the rat carotid artery injury model.

Several antagonists specific for platelet-derived growth factor (PDGF) or its receptors have recently been developed and shown to inhibit intimal hyperplasia formation in various animal models, but data investigating the durability of this intervention is limited. The present study was designed to investigate the potency of PDGF B-chain aptamer, a novel type of PDGF-AB and -BB antagonist, in the rat carotid model and to characterize intermediate-term effects on lesion formation. One hundred thirty-four animals were randomized to aptamer treatment or placebo. Daily treatment with the antagonist resulted in a 50% reduction in lesion size at 2 weeks (P<0.001). The beneficial effect involved increased apoptosis and possibly an interference with smooth muscle cell migration. Discontinuing administration 1 week earlier did not give any significant benefit compared with phosphate-buffered saline-treated controls. When the antagonist was administered for 2 weeks and the vessels analyzed 6 weeks later, the beneficial effect was lost and the treated lesions had a higher intima-media and area-cell ratio compared with the treated lesions in the 2-week-endpoint study. Our findings confirm a role of PDGF B-chain in intimal hyperplasia, but the successful use of PDGF antagonists may require either prolonged treatment or combination therapy with other agents.

Angioplasty, Balloon↗
PubMed2000

The course of severe chronic fatigue syndrome in childhood.

Little has been reported on prognostic indicators in children with chronic fatigue syndrome (CFS). We used interviews with children and parents, a mean of 45.5 months after illness onset, to follow up 25 cases of CFS referred to tertiary paediatric psychiatric clinics. At its worst, the illness had been markedly handicapping (prolonged bed-rest and school absence in two-thirds); mean time out of school was one academic year. Two-thirds, however, had recovered and resumed normal activities--mean duration of illness to recovery/assessment 38 months--and none had developed other medical conditions. Recovery was associated with specific physical triggers to the illness, with start of illness in the autumn school term and with higher socioeconomic status. Severe fatigue states in children can cause serious and longlasting handicap but most children recover.

Adolescent↗
PubMed2000

The orthopaedic management of peripheral ischaemia in meningococcal septicaemia in children.

Between March 1993 and February 1999, 14 children aged from eight months to 14.75 years were admitted to the paediatric intensive-care unit with meningococcal septicaemia in association with severe peripheral ischaemia. Of these, 13 were operated upon, eight of whom had early fasciotomies. Five children died. Of the nine survivors, one had no amputations while in the other eight 14 limb segments were amputated. We review the case histories and propose a protocol for the early management of these children.

Adolescent↗
PubMed1999

Cerberus regulates left-right asymmetry of the embryonic head and heart.

BACKGROUND: Most of the molecules known to regulate left-right asymmetry in vertebrate embryos are expressed on the left side of the future trunk region of the embryo. Members of the protein family comprising Cerberus and the putative tumour suppressor Dan have not before been implicated in left-right asymmetry. In Xenopus, these proteins have been shown to antagonise members of the transforming growth factor beta (TGF-beta) and Wnt families of signalling proteins. RESULTS: Chick Cerberus (cCer) was found to be expressed in the left head mesenchyme and in the left flank of the embryo. Expression on the left side of the head was controlled by Sonic hedgehog (Shh) acting through the TGF-beta family member Nodal; in the flank, cCer was also regulated by Shh, but independently of Nodal. Surprisingly, although no known targets of Cerberus are expressed asymmetrically on the right side of the embryo at these stages, misexpression of cCer on this side of the embryo led to upregulation of the transcription factor Pitx2 and reversal of the direction of heart and head turning, apparently as independent events. Consistent with the possibility that cCer may be acting on bilaterally expressed TGF-beta family members such as the bone morphogenetic proteins (BMPs), this result was mimicked by right-sided misexpression of the BMP antagonist, Noggin. CONCLUSIONS: Our findings suggest that cCer maintains a delicate balance of different TGF-beta family members involved in laterality decisions, and reveal the existence of partially overlapping molecular pathways regulating left-right asymmetry in the head and trunk of the embryo.

Amino Acid Sequence↗
PubMed1999

4G/5G promoter polymorphism in the plasminogen-activator-inhibitor-1 gene and outcome of meningococcal disease. Meningococcal Research Group.

BACKGROUND: Intravascular coagulation with infarction of skin, digits, and limbs is a characteristic feature of meningococcal sepsis. Children with meningococcal sepsis have higher than normal concentrations of plasminogen activator inhibitor 1 (PAI-1) in plasma. Combined with the widespread venous thrombosis, this finding suggests an impairment of fibrinolysis. A common functional insertion/deletion (4G/5G) polymorphism exists in the promoter region of the PAI-1 gene. We tested the hypothesis that children with the 4G/4G genotype produce higher concentrations of PAI-1, develop more severe coagulopathy, and are at greater risk of death during meningococcal sepsis. METHODS: The relation between meningococcal disease outcome, PAI-1 concentration, and PAI-1 genotype was investigated in 175 children with meningococcal disease (37 from Rotterdam, the Netherlands, and 138 from London, UK) and 226 controls (137 from Rotterdam, 89 from London). PAI-1 concentrations in plasma were measured by ELISA, and the 4G/5G PAI-1 polymorphism was detected by PCR and hybridisation. FINDINGS: Concentrations of PAI-1 on admission correlated with presentation (sepsis or meningitis) and outcome. The median PAI-1 concentration in children who died was substantially higher than that in survivors (2448 [IQR 1115-3191] vs 370 [146-914] ng/mL; p<0.0001). Patients with the 4G/4G genotype had significantly higher PAI-1 concentrations than those with the 4G/5G or 5G/5G genotype (1051 [550-2440] vs 436 [198-1225] ng/mL; p=0.03), and had an increased risk of death (relative risk 2.0 [1.0-3.8] for the two cohorts combined, and 4.8 [1.8-13] for the London cohort). INTERPRETATION: A genetic predisposition to produce high concentrations of PAI-1 is associated with poor outcome of meningococcal sepsis. This finding suggests that impaired fibrinolysis is an important factor in the pathophysiology of meningococcal sepsis.

Adolescent↗
PubMed1999

Association of variants of the gene for mannose-binding lectin with susceptibility to meningococcal disease. Meningococcal Research Group.

BACKGROUND: The reasons why meningococcal disease develops in only a small proportion of individuals carrying the causative bacteria are unknown. Differences in host responses to bacterial colonisation are thought to be involved, since people with deficiencies in the terminal components of the complement pathway, or of properdin, are susceptible to meningococcal disease. We postulate that genetic variants of mannose-binding lectin (MBL), a plasma opsonin that initiates another pathway of complement activation, might similarly cause susceptibility to meningococcal disease. METHODS: The frequency of variants of the MBL gene was ascertained in children with meningococcal disease and controls from two independent studies; one hospital-based (194 patients and 272 controls [patients with non-infectious disorders]), and one community-based (72 patients and 110 controls [healthy individuals]), by means of PCR and restriction-enzyme digestion, with confirmation by DNA sequencing. FINDINGS: The proportion of people homozygous for MBL-variant alleles was higher in patients with meningococcal disease than in controls in the hospital study (15 [7.7%] vs four [1.5%]; odds ratio 6.5 [95% CI 2.0-27.2]) and in the community study (six [8.3%] vs three [2.7%]; 4.5 [0.9-29.1]). The population attributable fraction of cases attributable to MBL variants (homozygous and heterozygous) was 32%. INTERPRETATION: The MBL pathway is a critical determinant of meningococcal-disease susceptibility, and genetic variants of MBL might account for a third of all disease cases.

Adolescent↗