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PubMed2002

["Natural cause of death or not?" How do nursing home physicians act when in doubt of natural cause of death?].

The objective of the study was to explore if nursing home physicians act by law, when they doubt the natural cause of death. In May 1999, a questionnaire was sent to 153 nursing home physicians in the region of Utrecht and Nijmegen. They were asked if they consult the coroner when they have doubts about the natural cause of death. Eighty-six percent (104) returned the questionnaire. Thirty-two percent of the nursing home physicians always consult the coroner and 52% does so most of the time. Only 12% does not consult the coroner most of the time and 2% never does. The main reasons for not consulting the coroner were that nursing home physicians judge a death after a fall as an incident that fits in the descending lifeline of patients and that some nursing home physicians had bad experiences consulting the coroner. We conclude that this policy may lead to underregistration of unnatural deaths. Changing the definition or changing the law may reduce this problem. Education and information can also contribute to change in physician's attitudes.

Accidents↗
PubMed1989

[Cause od death statistics and death certificate documentation. 1. Historical development of cause of death statistics of fetal death, infants and children and current regulations in the GDR].

After having described the beginnings of documentation and statistics of causes of death of newborns and children the development of this branch of medical statistics in the GDR and the introduction of a special death certificate in 1961 is dealt with. To help obstetricians, perinatologists and pediatrists to tackle the problem of documentation of the causes of death of stillborns and newborns the 9th revision of ICD, the nowadays valid death certificate and special rules of signing are explained to avoid mistakes, which are often met with in the daily practice.

Cause of Death↗
PubMed1994

High concentrations of fibronectin fragments cause short-term catabolic effects in cartilage tissue while lower concentrations cause continuous anabolic effects.

We reported earlier that Fn fragments (Fn-f) added to bovine articular cartilage cultured in serum-free DMEM cause marked elevated release of protease activity within a few days. This results in greatly elevated rates of release of proteoglycan (PG). We have now extended our studies to 4-week cultures of cartilage in the presence of 10% serum. We report here that cartilage cultured with 0.01, 0.1, and 1 microM of an amino terminal 29-kDa Fn-f in 10% serum accelerated the loss of PG from the tissue during the first few days in a concentration-dependent manner. However, beyond this period PG content decreased much more slowly. During this early period, the 29-kDa Fn-f decreased rates of protein and PG synthesis up to 50% in a concentration-dependent fashion. Beyond this period, the synthesis rates began to increase in a mode inversely related to 29-kDa Fn-f concentration, up to 135% of Fn-f free control values. However, during the entire culture period, cartilage cultured with 1 nM 29-kDa Fn-f had higher PG contents and had enhanced rates of protein and PG synthesis. Since 1 nM 29-kDa Fn-f stabilized cartilage against decreases in PG content, we tested its ability to block the activity of higher 29-kDa Fn-f concentrations. Cartilage was preincubated for 7 days with 1 nM 29-kDa Fn-f, and then the culture adjusted to 100 nM 29-kDa Fn-f to cause PG depletion. The preincubated cartilage showed markedly enhanced resistance to PG depletion. Since the protective effect was similar to known properties of IGF-1, the ability of 20 ng/ml IGF-1 to block against the effects of 100 nM Fn-f was tested and shown to be similar in magnitude to that of 1 nM 29-kDa Fn-f. We propose that the initial catabolic effects of higher concentrations of Fn-f, followed by the later anabolic effects, may aid in tissue repair. Also, the continuous anabolic effects of lower concentrations may be involved in tissue homeostasis.

Amino Acid Sequence↗
PubMed1994

Five novel point mutations: two causing haemophilia B and three causing factor X deficiency.

Factors IX and X are plasma glycoproteins important in the middle phase of the coagulation cascade, and a bleeding disorder of variable severity results from abnormalities in the expression of either gene encoding these proteins. Nearly 380 unique molecular mechanisms cause factor IX deficiency, or haemophilia B, but only a limited number of mutations causing congenital factor X deficiency have been characterized to date. In this study enzymatic amplification has been used to examine the molecular basis for factor IX deficiency in two patients and factor X deficiency in two patients. Genomic DNA was isolated from each patient and synthetic oligonucleotide primers were used in the polymerase chain reaction to amplify each exon, splice junction and polyadenylation site. Amplified DNA was then cloned into pUC18 and sequenced. Five novel point mutations were identified, two occurring in the eighth exon of the factor IX gene and three in the eighth exon of the factor X gene. One of the haemophilia B mutations and one of the factor X mutations altered homologous histidine residues near the serine of the catalytic triad.

Base Sequence↗
PubMed2001

A comparison between septic bursitis caused by Staphylococcus aureus and those caused by other organisms.

Septic bursitis is an infection that usually involves olecranon and prepatellar bursae. Staphylococcus aureus is responsible for around 80% of cases. However, information regarding bursitis caused by non-Staphylococcus aureus microorganisms (NSAB) is scant. In this paper we describe the characteristics of NSAB and emphasise differences between these and Staphylococcus aureus bursitis (SAB). A retrospective study of all cases with septic bursitis seen between January 1991 and June 1998 at one university hospital was conducted. Only cases in which bursal fluid culture yielded growth of a microorganism were analysed. A literature review was conducted for completeness. Fifty-seven episodes of septic bursitis in 56 patients were studied: 47 of these were caused by Staphylococcus aureus and 11 by non-Staphylococcus aureus microorganisms. Forty-three SAB patients were male (91%). Mean age at diagnosis was 50 years (range 20-85 years). The presentation of bursitis had a seasonal trend, with a peak in the summer. Twenty-three patients (51%) had occupations involving frequent or sustained pressure on the bursae. Other risk factors were recent trauma in 11 (23%), alcoholism in six (13%), pre-existing bursal disease in five (11%), and chronic obstructive pulmonary disease in four (9%). There were 20 cases of olecranon bursitis (43%), 25 of prepatellar bursitis (53%) and two of first metatarsophalangeal bursitis. Characteristics of patients from the literature review were similar. Eight NSAB patients (73%) were male. Mean age at diagnosis was 46.9 (range 29-83 years). Two patients were plumbers and one a stonemason. Five (45%) had neither putative systemic nor local risk factors. There were five olecranon (45%), five prepatellar (45%), and one external malleolus bursitis. Infection by a mixed flora was common. Unlike SAB, the presentation of cases did not have a seasonal trend. The clinical spectrum of non-Staphylococcus aureus bursitis (NSAB) differs from that of Staphylococcus Aureus bursitis (SAB), and this should be considered in the initial diagnosis of septic bursitis.

Adult↗
PubMed1987

Diacylglycerol causes Ca release from the platelet dense tubular system: comparisons with Ca release caused by inositol 1,4,5-triphosphate.

Platelet activation is often associated with an increase in the cytosolic free Ca concentration that is due in part to Ca release from the dense tubular system. The present studies examine whether the diacylglycerol formed by phosphoinositide hydrolysis during platelet activation contributes to this process. The effect of diacylglycerol on the dense tubular system was tested using platelets that were permeabilized with saponin and then allowed to accumulate 45Ca. A synthetic diacylglycerol, 1-oleoyl-2-acetoyl glycerol (OAG), released up to 70% of the ionophore A23187-releasable 45Ca, a fraction identical to that discharged by inositol 1,4,5-triphosphate (IP3) under the same conditions. 45Ca release was half-maximal at 40 microM OAG and 1 microM IP3. The response to OAG was not inhibited by aspirin and could not be reproduced by the addition of a phorbol ester, which suggests that it involves neither arachidonic acid metabolism nor protein kinase C activation. The time course of OAG-induced 45Ca release, which was slower than IP3-induced 45Ca release, corresponded to the time course of conversion of the OAG to 1-oleoyl-2-acetoyl phosphatidic acid (OAG-PA). When either OAG-PA or lysophosphatidic acid was added to the saponin-treated platelets, the extent of 45Ca release was similar to that observed with OAG, but both the OAG-PA and the lysophosphatidic acid were 5 to 10 times more potent than OAG on a molar basis. These data suggest: that the Ca release caused by diacylglycerol is actually due to formation of phosphatidic acid and/or lysophosphatidic acid, that these molecules are not acting as simple Ca ionophores and that diacylglycerol metabolites may augment the changes in Ca homeostasis caused by IP3 during platelet activation.

Adenosine Triphosphate↗
PubMed1985

Hydrogen peroxide causes dimethylthiourea consumption while hydroxyl radical causes dimethyl sulfoxide consumption in vitro.

Addition of increasing concentrations of hydrogen peroxide (H2O2) caused progressive decreases in dimethylthiourea (DMTU) concentrations which were inhibitable by simultaneous addition of catalase, but not the superoxide anion (O2-.) scavenger, superoxide dismutase (SOD), or hydroxyl radical (.OH) scavengers, such as mannitol, sodium benzoate or dimethyl sulfoxide (DMSO). In parallel, addition of increasing concentrations of H2O2 with FE++/EDTA (but not H2O2 alone) caused decreases in DMSO concentrations which were inhibitable by simultaneous addition of .OH scavengers but not SOD or catalase. Addition of DMTU, but not DMSO, also decreased H2O2 concentrations in vitro. The results indicate the relative scavenging specificities of DMTU and DMSO for H2O2 and .OH, respectively. The findings also suggest that measurement of DMTU or DMSO consumption could help assess the contribution of O2 metabolites in biological systems.

Chromatography, Gas↗
PubMed2000

Regulatory problems caused by contamination, a frequently overlooked cause of veterinary drug residues.

The occurrence of violative residues of veterinary medicines and other, unauthorised, drugs in food of animal origin is an issue of popular concern within the European Union. Violations can occur as a result of improper use of a licensed product or through the illegal use of an unlicensed substance. However, a "violative" analytical result does not necessarily mean that abuse has occurred. Contamination of animal feedingstuffs, environmental contamination and animal-to-animal transfer of drugs can also cause residue violations. This paper reviews these inadvertent causes of residues violations in food, and includes data generated using chromatographic and non-chromatographic methods of analysis.

Animals↗
PubMed1983

Injuries caused by plastic bullets compared with those caused by rubber bullets.

The injuries sustained by 99 people struck by plastic bullets, were compared with those sustained by 90 people struck by rubber bullets. Plastic bullets struck the head and chest less often than rubber bullets and caused fewer serious injuries to the face and chest, but tended to cause more serious skull and brain injuries.

Adult↗
PubMed1997

Acquired protein S and antithrombin III deficiency caused by nephrotic syndrome: an unusual cause of graft thrombosis.

Thrombotic phenomena are well-recognized complications of nephrotic syndrome attributable to loss of intermediate-sized antithrombotic proteins in the urine, resulting in a hypercoaguable state. As such, nephrotic syndrome may be associated with a reduction in circulating antithrombin III and free protein S levels. Associated spontaneous thrombotic complications are generally venous in nature, with arterial thrombosis occurring less frequently. Hypercoagulability caused by acquired nephrotic syndrome has not generally been recognized as a cause of acute thrombosis of arterial bypass grafts. We report two patients who after having nephrotic syndrome sustained acute thrombosis of their arterial bypass grafts. Pathogenesis and management are discussed.

Antithrombin III Deficiency↗
PubMedDate not supplied

Cause of long thoracic nerve palsy: a possible dynamic fascial sling cause.

Long thoracic nerve palsy can result from sudden or repetitive external biomechanical forces. This investigation describes a possible dynamic cause from internal forces. Six fresh cadaveric shoulders (3 female, 3 male, 4 left, 2 right) with full range of motion were systematically dissected to evaluate the anatomic course of the long thoracic nerve. In all specimens a tight fascial band of tissue arose from the inferior aspect of the brachial plexus, extended just superior to the middle scalene muscle insertion on the first rib, and presented a digitation that extended to the proximal aspect of the serratus anterior muscle. With progressive manual abduction and external rotation, the long thoracic nerve was found to "bow-string" across the fascial band. Medial and upward migration of the superior most aspect of the scapula was found to further compress the long thoracic nerve. Previous investigations have reported that nerves tolerate a 10% increase in their resting length before a stretch-induced neuropraxia develops. Previous studies postulated that long thoracic nerve palsy resulted from the tethering effect of the scalenus medius muscle as it actively or passively compressed the nerve; however, similar neuromuscular relationships occur in many other anatomic sites without ill effect. We propose that the cause of long thoracic nerve palsy may be this "bow-stringing" phenomenon of the nerve across this tight fascial band. This condition may be further exacerbated with medial and upward migration of the superior aspect of the scapula as is commonly seen with scapulothoracic dyskinesia and fatigue of the scapular stabilizers. Rehabilitation for long thoracic nerve palsy may therefore benefit from special attention to scapulothoracic muscle stabilization.

Adult↗
PubMed2001

A large outbreak of conjunctivitis caused by a single genotype of Neisseria gonorrhoeae distinct from those causing genital tract infections.

Several epidemics of gonococcal conjunctivitis have occurred in Aboriginal populations in Central Australia. In 1997, the first outbreak in the Kimberley region of Western Australia occurred, spreading to Central Australia with a total of 447 cases. A genotyping method was applied directly to DNA extracted from patient samples to characterize the gonococcus causing the epidemic and to compare it with contemporaneous genital isolates. Those positive conjunctival specimens from Kimberley and Central Australia that could be genotyped were all indistinguishable, but were distinct from the genital gonococci, even when they shared the same auxotype and serotype. This suggested that the outbreak was due to a single genotype of Neisseria gonorrhoeae that had probably been carried between communities by infected individuals. We did not find evidence to support the existence of a genital reservoir of the types causing epidemic gonococcal conjunctivitis.

Adolescent↗
PubMed2003

Gadolinium susceptibility artifact causing false positive stenosis isolated to the proximal common carotid artery in 3D dynamic contrast medium enhanced MR angiography of the thorax--a brief review of causes and prevention.

Due to the close proximity of arteries and veins in the superior mediastinum and upper extremities, T2* shortening effects of the gadolinium within the central veins may cause artifactual vascular stenosis (susceptibility artifact) on arterial-phase MR angiographic images of the major branches of the aortic arch. We report a case of artifactual stenosis isolated to the origin of the left common carotid artery on arterial-phase MR angiography, secondary to susceptibility artifact from non-diluted gadolinium in the adjacent brachiocephalic vein. The cause of the artifact, its identification and prevention is reviewed.

Adult↗
PubMed2001

Atrichia caused by mutations in the vitamin D receptor gene is a phenocopy of generalized atrichia caused by mutations in the hairless gene.

Generalized atrichia with papules is a rare disorder characterized by loss of hair shortly after birth and development of cutaneous cysts. Mutations in the hairless gene (HR) cause this phenotype in both mouse and human. Here we present a case of atrichia with papules in a patient with a normal HAIRLESS gene but with mutations in both alleles of the VITAMIN D RECEPTOR. The patient exhibited vitamin D resistant rickets, which was confirmed by an absent response of her fibroblasts to 1,25-dihydroxyvitamin D3 in vitro. Similar to individuals with HAIRLESS mutations, her skin showed an absence of normal hair follicles and the presence of follicular remnants and cysts. The cyst epithelium contained keratin-15- and keratin-17-positive cells suggesting derivation from the hair follicle bulge and the presence of epithelial stem cells. Although hair loss has been reported in association with hereditary vitamin D resistant rickets, we now characterize this alopecia as clinically and pathologically indistinguishable from generalized atrichia with papules, which was previously thought to be caused only by mutations in HAIRLESS. These findings suggest that VDR and HR, which are both zinc finger proteins, may be in the same genetic pathway that controls postnatal cycling of the hair follicle.

Alopecia↗
PubMed2001

BSE did not cause variant CJD: an alternative cause related to post-industrial environmental contamination.

The new prion diseases that have emerged in the last 15 years are bovine spongiform encephalopathy (BSE) and variant Creutzfeldt-Jakob disease (variant CJD). Although initially confined to the UK, these diseases have recently emerged in other European countries. The accepted cause of the human disease is that BSE spread from cattle to humans by the consumption of infected beef. However, the evidence that supports this is very thin. This article describes this evidence and lists a series of hypotheses concerning the cause of both BSE and variant CJD. The final hypothesis is based on recent evidence linking prion diseases to environmental factors including manganese. High environmental availability of manganese is associated with the prevalence of those prion diseases not linked to BSE. Therefore it is quite possible that BSE and variant CJD have emerged as a result of manganese-rich industrial pollution that has only occurred in the last century.

Animals↗
PubMed1989

[Inappropriate ADH secretion caused by alcohol withdrawal: a rare cause of hyponatremia].

A 52-year-old man, known to be alcohol dependent, was admitted to hospital because of intense drowsiness. He had previously drunk over 100 g alcohol daily, but for the last 2 days "not a drop". Serum sodium concentration was 103 mmol/l, serum osmolarity was low (216 mosmol/l) and urine osmolarity remarkably high (373 mosmol/l). These abnormalities, taken in conjunction with his normal water balance (absence of obvious edema or dehydration), suggested the diagnosis of inappropriate secretion of antidiuretic hormone (ADH), and this was confirmed by a water loading test. Exclusion of the recognized causes of inappropriate ADH secretion left alcohol withdrawal as the only tenable explanation. The reabsorption of water which it induced was the cause of the patient's hyponatraemia and drowsiness. Restriction of fluid intake to 500 ml daily with continued total abstinence from alcohol led to rapid recovery. The discovery of hyponatraemia in an alcoholic in a state of normal water balance should rouse suspicion of inappropriate ADH secretion.

Ethanol↗
PubMed1998

Hydrogen peroxide causes RAD9-dependent cell cycle arrest in G2 in Saccharomyces cerevisiae whereas menadione causes G1 arrest independent of RAD9 function.

This study shows differences at the level of cell cycle arrest between the response of yeast cells to hydrogen peroxide and superoxide stress. These include both cell cycle phases at which arrest occurs and the involvement of the RAD9 checkpoint gene. Wild-type and rad9 cells were treated with hydrogen peroxide or the superoxide-generating agent menadione. rad9 mutants were up to 100-fold more sensitive to hydrogen peroxide but not affected in their resistance to menadione. Hydrogen peroxide caused G2-phase arrest, whereas menadione-treated cells arrested in G1. G2 arrest, induced by methyl 2-benzimidazil carbamate, increased cellular resistance to hydrogen peroxide but not to menadione. G1 arrest mediated by alpha-factor caused an increase in survival of wild-type cells treated with menadione but not with hydrogen peroxide. A cdc28 mutant arrested in G1 was significantly more sensitive to hydrogen peroxide than other cdc mutants arrested in later phases, including G2. rad9 cells have normal stationary phase resistance to hydrogen peroxide, the ability to adapt to it, glutathione content and induction of genes via the stress responsive element. Although rad9-dependent G2 arrest is important, other rad9-dependent factors may be involved in the resistance of cells to hydrogen peroxide since arrest in G2 did not make rad9 cells fully resistant.

Benzimidazoles↗
PubMed2001

Selective resistance to parathyroid hormone caused by a novel uncoupling mutation in the carboxyl terminus of G alpha(s). A cause of pseudohypoparathyroidism type Ib.

G(s) is a heterotrimeric (alpha, beta, and gamma chains) G protein that couples heptahelical plasma membrane receptors to stimulation of adenylyl cyclase. Inactivation of one GNAS1 gene allele encoding the alpha chain of G(s) (G alpha(s)) causes pseudohypoparathyroidism type Ia. Affected subjects have resistance to parathyroid hormone (PTH) and other hormones that activate adenylyl cyclase plus somatic features termed Albright hereditary osteodystrophy. By contrast, subjects with pseudohypoparathyroidism type Ib have hormone resistance that is limited to PTH and lack Albright hereditary osteodystrophy. The molecular basis for pseudohypoparathyroidism type Ib is unknown. We analyzed the GNAS1 gene for mutations using polymerase chain reaction to amplify genomic DNA from three brothers with pseudohypoparathyroidism type Ib. We identified a novel heterozygous 3-base pair deletion causing loss of isoleucine 382 in the three affected boys and their clinically unaffected mother and maternal grandfather. This mutation was absent in other family members and 15 additional unrelated subjects with pseudohypoparathyroidism type Ib. To characterize the signaling properties of the mutant G alpha(s), we used site-directed mutagenesis to introduce the isoleucine 382 deletion into a wild type G alpha(s) cDNA, transfected HEK293 cells with either wild type or mutant G alpha(s) cDNA, plus cDNAs encoding heptahelical receptors for PTH, thyrotropic hormone, or luteinizing hormone, and we measured cAMP production in response to hormone stimulation. The mutant G alpha(s) protein was unable to interact with the receptor for PTH but showed normal coupling to the other coexpressed heptahelical receptors. These results provide evidence of selective uncoupling of the mutant G alpha(s) from PTH receptors and explain PTH-specific hormone resistance in these three brothers with pseudohypoparathyroidism type Ib. The absence of PTH resistance in the mother and maternal grandfather who carry the same mutation is consistent with current models of paternal imprinting of the GNAS1 gene.

Base Sequence↗