Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “causes”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 145 records · Page 8Linked to original sources
PubMed1980

[Clinical differentiation between idiopathic respiratory distress, neonatal septicemia caused by group B streptococci and septicemia caused by other pathogens (author's transl)].

Since bacterial infection in newborns must be treated as specifically and as early as possible, it is important to confirm a diagnosis of suspected infection based on clinical symptoms and to take possible pathogens into consideration when choosing therapy. RDS and septicemia with Group B streptococci can present very similar clinical symptoms, but leucopenia on the first day of life is most probably an indication of septicemia with Group B streptococci. Septicemia caused by other pathogens, however, usually has a much later onset. In the days following birth a raised cardiothoracic index indicates RDS. Other differential criteria are being investigated.

Candida albicans↗
PubMed1996

G3P2 rotaviruses causing diarrhoeal disease in neonates differ in VP4, VP7 and NSP4 sequence from G3P2 strains causing asymptomatic neonatal infection.

During longitudinal epidemiological studies of rotavirus infections in children in Melbourne, Australia human G3P2 rotavirus strains causing asymptomatic or symptomatic infections have been identified. Eleven strains (AS strains) associated with asymptomatic infection of newborn babies from 1974-1984, and five strains (S strains) associated with symptomatic infection of newborn babies (4) or a 22 week old infant (1) during 1980-1986 were studied. The entire nucleotide sequences of genes coding for VP4, VP7, NSP4 and VP6 were derived for representative AS and S strains. The nucleotide sequences of neutralization epitope regions present on the outer capsid proteins VP4 and VP7 (regions C and F) showed extensive conservation of nucleotide and deduced amino acid sequence in all strains. Minor variations were observed over the 12 year period in VP7 epitope regions A and B in some strains. Specific conserved amino acids differences between the asymptomatic and symptomatic strains were observed in the genes encoding VP4 at aa133 and 303 (asparagine or threonine) and 380 (serine or isoleucine), VP7 at aa27 (threonine or isoleucine), aa29 (isoleucine or threonine), aa42 (valine or alanine) and aa238 (asparagine or aspartic acid/serine) and NSP4 at aa135 (isoleucine or valine). No amino acid changes were identified in gene 6. The observed amino acid differences occurred in proteins that have been implicated in virulence, and correlate with differences in clinical symptoms of infants infected with these strains. These results permit speculation about the genetic basis for virulence of human strains.

Amino Acid Sequence↗
PubMed1980

Comparison between predicted cause of death and cause of death found at autopsy in medicolegal autopsy material.

The question whether an autopsy could have been omitted without adversely affecting diagnostic accuracy in cases in which an unnatural death was not suspected, was investigated by evaluating data from the files of cases handled in 1977 at the Government Department of Forensic Medicine in Uppsala in which the police had requested a simple medicolegal examination. The police report and the result of an external examination were evaluated blindly and cases divided into three groups. In 95 cases (12%) no autopsy, in 360 cases (45%) a partial autopsy, and in 346 cases (43%) a complete autopsy was considered necessary. In three of the 95 cases and in four of the 360 cases a wrong diagnosis was made. In 59 cases (7%) a complete medicolegal examination was performed. In 21 of the latter the circumstances of death were obscure and in 11 of these an unnatural cause of death was found. The investigation confirms that all cases must be handled by skilled medicolegal experts, that the extent of the medicolegal examination can well be assessed by the physician in charge, and that the autopsy procedure can be simplified in many cases and omitted in some, especially in a situation where resources are limited, without significantly affecting diagnostic accuracy in the individual case. However this policy adversely affects scientific studies on larger autopsy material.

Autopsy↗
PubMed1994

Cardiovascular causes of loss of consciousness in patients with presumed epilepsy: a cause of the increased sudden death rate in people with epilepsy?

UNLABELLED: BACKGROUND, METHODS, AND RESULTS: Syncope and seizures are often indistinguishable clinically. We present a series of 12 patients diagnosed as having epilepsy. Despite normal or nonspecific electroencephalographic findings, 11 of 12 patients were treated or offered treatment with long-term anticonvulsant agents. Subsequently, diagnoses of arrhythmic or neurally mediated syncope were made in all patients using Holter monitoring, long-term ambulatory loop electrocardiographic recording, or tilt-table studies. Arrhythmias included torsades de pointes (four patients), atrioventricular nodal reentrant supraventricular tachycardia (one patient), and sinus arrest (two patients). The remaining five patients had neurally mediated syncope with hypotension and bradycardia, including asystole in two patients. Treatment for the documented cardiovascular abnormalities resulted in the alleviation of syncopal symptoms. CONCLUSIONS: Because the observed cardiovascular abnormalities are potentially fatal, this series suggests that undiagnosed cardiac syncope may contribute to the documented increased sudden death rate in patients with presumed epilepsy. Cardiac causes of loss of consciousness should be considered in patients with presumed epilepsy, atypical premonitory symptoms (such as nausea, lightheadedness, or palpitations), nondiagnostic electroencephalograms, and failure to respond to anticonvulsant therapy.

Adolescent↗
PubMed1994

High doses of oxytocin cause sedation and low doses cause an anxiolytic-like effect in male rats.

The aim of the present investigation was to explore dose relationships for effects of oxytocin on spontaneous motor activity in the rat. Oxytocin in doses from 1-1000 micrograms/kg was given SC to male Sprague-Dawley rats, and spontaneous motor behavior was measured by means of photocell-operated open-field observations. In the rats treated with low doses of oxytocin (1-4 micrograms/kg), there was a decrease in peripheral locomotor activity. With increasing doses (250-1000 micrograms/kg), there were clear signs of sedative effects as indicated by a suppression of locomotor activity and rearing. The time course for the effect of oxytocin on peripheral activity (1 microgram/kg) and rearing (1 mg/kg) was tested. A maximal effect was obtained within 1 h and, thereafter, the behavior gradually returned to normal within 24 h. This spectrum of effects caused by oxytocin was similar to that of midazolam but different from that induced by raclopride.

Animals↗
PubMed1993

Stanozolol causes rapid pain relief and healing of cutaneous ulcers caused by cryofibrinogenemia.

BACKGROUND: Cutaneous manifestations of cryofibrinogenemia include purpura, ecchymosis, and ulcerations. The histology of these lesions is characterized by intravascular thrombi. OBJECTIVE: Our purpose was to test the efficacy of stanozolol, a drug capable of fibrinolytic enhancement, in treating cutaneous ulcers caused by cryofibrinogenemia. METHODS: Eight patients with cutaneous ulcerations from cryofibrinogenemia were treated with stanozolol. Plasma cryofibrinogen was measured before and during treatment with stanozolol. Histologic evaluation was also performed before treatment and in selected patients during treatment. RESULTS: After treatment, seven of the eight patients had healing of their ulcers, prompt reduction in their pain, and improvement in livedo reticularis and purpura. Four of the eight patients had no detectable plasma cryofibrinogen after treatment. In addition, dermal intravascular thrombi resolved. Stanozolol was well tolerated and had minimal side effects. CONCLUSION: We conclude that stanozolol is a safe and effective treatment of the cutaneous manifestations of cryofibrinogenemia.

Adult↗
PubMed2005

Perceptual speed does not cause intelligence, and intelligence does not cause perceptual speed.

There is ongoing debate whether the efficiency of local cognitive processes leads to global cognitive ability or whether global ability feeds the efficiency of basic processes. A prominent example is the well-replicated association between inspection time (IT), a measure of perceptual discrimination speed, and intelligence (IQ), where it is not known whether increased speed is a cause or consequence of high IQ. We investigated the direction of causation between IT and IQ in 2012 genetically related subjects from Australia and The Netherlands. Models in which the reliable variance of each observed variable was specified as a latent trait showed IT correlations of -0.44 and -0.33 with respective Performance and Verbal IQ; heritabilities were 57% (IT), 83% (PIQ) and 77% (VIQ). Directional causation models provided poor fits to the data, with covariation best explained by pleiotropic genes (influencing variation in both IT and IQ). This finding of a common genetic factor provides a better target for identifying genes involved in cognition than genes which are unique to specific traits.

Adolescent↗
PubMed2005

Comparative study of Escherichia coli virulence determinants in strains causing urinary tract bacteremia versus strains causing pyelonephritis and other sources of bacteremia.

To assess the role of phylogenetic background and putative virulence factors (VFs) in Escherichia coli causing urinary bacteremia, 50 strains isolated from this condition were compared with 50 strains isolated from pyelonephritis and 50 from other sources of bacteremia. papA and papGII were significantly more prevalent in urinary bacteremia and pyelonephritis (78%, 66% and 70%, 58%) than in other-source bacteremia (48% and 24%), whereas sfa/focDE and cnf1 were more prevalent in urinary-source bacteremia (56% and 44%) than in pyelonephritis and other-source bacteremia (28%, 42% and 20%, 28%). Group B2 was the most frequent in all conditions (63% of isolates) and exhibited the greatest concentration of VFs. Urinary tract bacteremia, pyelonephritis, and other-source bacteremia isolates presented similar virulence scores (7.8, 7.0, and 6.6); however, there were striking differences among the phylogenetic groups (8.7 in group B2 versus 3.4 in group A; P < .001). Group A and B1 strains almost exclusively infected compromised hosts.

Bacteremia↗
PubMed2006

Giant true saphenous vein graft aneurysm causing cardiac compression: a rare cause of atrial flutter.

A 67 year old man presented with new-onset atrial flutter. He had a history of coronary artery bypass graft (CABG) surgery on two occasions. Subsequent investigation revealed the presence of a large saphenous vein graft (SVG) aneurysm compressing the right heart. We postulate that the SVG aneurysm was the precipitating cause for the atrial flutter. This case is the first in the literature to document an atrial arrhythmia as the presenting feature of a SVG aneurysm.

Aged↗
PubMed2006

Senataxin, the yeast Sen1p orthologue: characterization of a unique protein in which recessive mutations cause ataxia and dominant mutations cause motor neuron disease.

A severe recessive cerebellar ataxia, Ataxia-Oculomotor Apraxia 2 (AOA2) and a juvenile onset form of dominant amyotrophic lateral sclerosis (ALS4) result from mutations of the Senataxin (SETX) gene. To begin characterization this disease protein, we developed a specific antibody to the DNA/RNA helicase domain of SETX. In murine brain, SETX concentrates in several regions, including cerebellum, hippocampus and olfactory bulb with a general neuronal expression profile, colocalizing with NeuN. In cultured cells, we found that SETX was cytoplasmically diffuse, but in the nucleus, SETX was punctate, colocalizing with fibrillarin, a marker of the nucleolus. In differentiated non-cycling cells, nuclear SETX was not restricted to the nucleolus but was diffuse within the nucleoplasm, suggesting cell-cycle-dependent localization. SETX missense mutations cluster within the N-terminus and helicase domains. Flag tagging at the N-terminus caused protein mislocation to the nucleoplasm and failure to export to the cytoplasm, suggesting that the N-terminus may be essential for correct SETX localization. We report here the first characterization of SETX protein, which may provide future insights into a new mechanism leading to neuron death.

Adult↗
PubMed2006

Mutation of the Myxoma virus SERP2 P1-site to prevent proteinase inhibition causes apoptosis in cultured RK-13 cells and attenuates disease in rabbits, but mutation to alter specificity causes apoptosis without reducing virulence.

Myxoma virus (MYX) prevents apoptosis in RK-13 cells and forms thick dermal lesions with 100% mortality in rabbits. MYX encodes the virulence factor SERP2, a serine proteinase inhibitor (serpin). SERP2 was mutated to evaluate SERP2 function during MYX infection. MYXDeltaSERP2::lacZ (deleted for SERP2) did not inhibit apoptosis in RK-13 cells; infected rabbits had thin dermal lesions and <10% mortality. MYX-SERP2-D294A, a P1-site aspartate to alanine mutant, inactivated the serpin; infection was indistinguishable from MYXDeltaSERP2::lacZ. SERP2-D294E prevented inhibition of caspase-8, caspase-10 and granzyme-B; and MYX-SERP2-D294E failed to block apoptosis in RK-13 cells, but was fully virulent in rabbits. MYXDeltaSERP2::crmA expressed crmA instead of SERP2 and inhibited apoptosis in cell culture, but caused thin lesions and only 70% mortality in rabbits, hence crmA cannot fully substitute for SERP2. Control of apoptosis in culture does not correlate with virulence in rabbits. Virulence may instead depend on inhibition of proinflammatory proteinases by SERP2.

Animals↗
PubMed1997

Age-related decline in humoral immunity caused by the selective loss of TH cells and decline in cellular immunity caused by the impaired migration of inflammatory cells without a loss of TDTH cells in SAMP1 mice.

We investigated the cellular basis of the age-related decline in antibody (Ab) and delayed-type hypersensitivity (DTH) responses to sheep red blood cells (SRBC) in vivo in short-lived senescence-accelerated mouse (SAM) P1. In SAMP1 mice, age-related decreases in CD4+ T cells in the peripheral blood occurred earlier than in control mice and occurred in parallel with the age-related decline in Ab and DTH responses. In addition, the involution of the thymus was faster. The injection of thymic T cells from young mice before sensitization completely restored the Ab responses in aged SAMP1 mice. These data suggest that the age-related decline in Ab response is due to the age-related early loss of helper-T (TH) cells. On the other hand, the local transfer of spleen cells from sensitized aged donors into the footpads of naive syngeneic recipients evoked strong DTH responses, demonstrating the existence of DTH-mediating T (TDTH) cells in the spleens of aged SAMP1 mice. Moreover, the local injection of naive spleen cells from young donors, together with the antigen, into the footpads caused DTH responses in sensitized aged recipients. These findings indicate that TDTH cells were induced and were able to migrate and function as effector cells in aged mice. When naive spleen cells from aged donors were injected locally into the footpad, they restored the DTH response in aged mice, but this effect did not work if the cells were injected intravenously. This demonstrates that the inflammatory cells of the aged mice were able to work at the local site, but could not migrate there. The intravenous injection of naive spleen cells from young donors restored the DTH response in aged mice, suggesting that the endothelial cells of aged mice were not impaired and permitted the inflammatory cells to migrate into the extravascular tissues. Thus, although the age-related decline of the Ab and DTH responses occur in parallel, we found different effects of aging on TH and TDTH cells in SAMP1 mice. Furthermore, our data suggest that the reason for the low DTH response in aged SAMP1 mice is not the loss of TDTH cells, but rather the impaired migration of inflammatory cells into the local site.

Aging↗
PubMed2002

Rarer causes of radiculopathy: spinal tumors, infections, and other unusual causes.

For the physiatrist practicing musculoskeletal medicine, patients with radiculopathy are a challenging and rewarding population for whom to provide care. Despite the rarity of diseases discussed in this article, at some time in his or her career every musculoskeletal physiatrist will see patients with these diagnoses as the cause of radiculopathy or back pain. A high index of suspicion is necessary to identify these rare disease processes accurately and promptly. The patient's history, examination, and plain-film radiographic evaluations remain the best tools with which to establish a differential and working diagnosis. The most important services that the physiatrist can provide to these patients are an astute application of the differential diagnosis to identify the specific etiology and the leadership required to organize a multi-disciplinary team of specialists to address all of the patient's needs.

Bone Diseases, Infectious↗
PubMed1996

Oligomycin sensitivity conferring protein of mitochondrial ATP synthase: deletions in the N-terminal end cause defects in interactions with F1, while deletions in the C-terminal end cause defects in interactions with F0.

The structure/function relationships of oligomycin sensitivity conferring protein (OSCP) of bovine mitochondrial ATP synthase were studied by nested deletion mutagenesis, followed by analyses of the resultant OSCPs for their ability to restore partial reactions of ATP synthesis in OSCP-depleted F1-F0 complexes. Our results indicate that, from the N-terminus of OSCP, up to 13 amino acid residues could be deleted without any effect on OSCP coupling activity. However, deletion of 16 or more residues led to a slow decline in the ability of resultant mutant forms to restore ATP synthesis. Compared to the wild-type form of OSCP, deletion mutant ND-28 (deletion of residues 1-28) is 50% as active in its ability to reconstitute ATP-Pi exchange activity. Detailed analyses of mutant ND-28 revealed that it was able to bind to the membrane segment (F0) of ATP synthase and restore oligomycin-sensitive ATPase activity in OSCP-depleted F1-F0 complexes. However, it did not bind to soluble segment F1, nor did it confer cold stability to either soluble F1 or reconstituted F1-F0 complex. On the other hand, studies on nested deletions on the C-terminal end indicate that three residues could be deleted without compromising the energy-coupling activity of OSCP. However, truncations of five or more residues caused an impairment in the ability of resultant mutant forms to restore ATP-Pi exchange activity in OSCP-depleted complexes. Mutant CD-10 (deletion of amino acids 181-190) was completely ineffective as a coupling factor. Detailed analyses of this mutant revealed that the subunit was able to bind to soluble F1 segment and confer cold stability to the enzyme but was neither able to associate with the membrane segment (F0) nor able to reconstitute high oligomycin sensitivity in depleted F1-F0 complexes. We take these data to suggest that the N-terminal end of OSCP corresponding to residues G16-N28 is essential for binding of the coupling factor to soluble F1 but not for coupling the energy of proton translocation to the synthesis of ATP; on the other hand, the carboxyl-terminal end of OSCP containing amino acids K181-M186 is important for F0-OSCP interactions as well as for the coupling of the energy of delta microH+ during the synthesis of ATP. These results suggest a model for OSCP in which the N-terminus is associated with the F1 segment and the C-terminus is associated with the F0 segment, while the central part of the polypeptide forms three or more helices constituting the stalk in the intact F1F0 enzyme.

Adenosine Triphosphatases↗
PubMed2002

Deoxynivalenol-nonproducing fusarium graminearum causes initial infection, but does not cause disease spread in wheat spikes.

Fusarium graminearum is a major pathogen that causes fusarium head blight (FHB) in wheat and produces deoxynivalenol (DON) in infected grain. In previous studies, the trichodiene synthase gene (Tri5) in the fungal strain GZ3639 was disrupted to produce the DON-nonproducing strain GZT40. In this report, the virulence of strains GZ3639 and GZT40 was tested on wheat cultivars with various resistance levels by using methods of spray inoculation and injection inoculation with fungal conidia. Under field and greenhouse conditions, strain GZ3639 produced significantly more disease symptoms and reduced more yield than strain GZT40 in all wheat cultivars tested. Conidia of strain GZT40 germinated and infected inoculated spikelets, but disease symptoms were limited to inoculated spikelets without spread to uninoculated spikelets. When strain GZT40 was inoculated using the spray method, multiple initial infection sites in a spike resulted in higher levels of disease symptoms than in spikes inoculated by a single injection. Greenhouse tests confirmed that strain GZT40 did not produce DON in the infected kernels following either inoculation method. The results confirm that DON production plays a significant role in the spread of FHB within a spike, and are the first report that DON production is not necessary for initial infection by the fungus.

Fusarium↗
PubMed1999

IgG titer, subclass, and light-chain phenotype of pregnancy-induced HPA-5b antibodies that cause or do not cause neonatal alloimmune thrombocytopenia.

BACKGROUND: The most common pregnancy-induced platelet-specific antibody is HPA-5b. Neonatal alloimmune thrombocytopenia that results from anti-HPA-5b may cause severe hemorrhage in only a few infants, but the sequelae for the affected children can be severe. It is therefore essential that infants at risk for neonatal alloimmune thrombocytopenia are identified. STUDY DESIGN AND METHODS: The IgG titer, subclass, and light-chain composition of pregnancy-induced anti-HPA-5b were determined by the monoclonal antibody-specific immobilization of platelet antigens assay. Sera were from 12 mothers, who among them had 16 pregnancies that resulted in an HPA-5-mismatched fetus (positive for HPA-5b). Eight mothers gave birth to an infant with a normal platelet count. Three maternal sera were obtained after delivery of a severely thrombocytopenic infant. Three alloimmunized women were followed repeatedly during the course of a subsequent pregnancy, again with an HPA-5-mismatched infant. RESULTS: There was no difference in the antibody titer or its subclass in mothers who had a thrombocytopenic child and the titer or subclass in mothers compared with those who had a child with a normal platelet count. All pregnancy-induced HPA-5b antibodies were of a predominant, lambda, light-chain type. The IgG subclass did not change during pregnancy. CONCLUSION: Neither the antibody titer nor the subclass composition predict the occurrence of thrombocytopenia in a newborn whose mother is alloimmunized against HPA-5b.

Antigens, Human Platelet↗
PubMed1984

[Inflammatory eye changes in the mouse caused by herpesvirus. Changes caused by the cytopathogenic effect. An animal model].

The reproducible inflammatory changes caused by infection with herpes simplex virus (Eidolon-Virus) in the anterior segment in mice represent a useful model. They are very similar to severe inflammation of the eye, as seen in herpes simplex infection. The method used by the authors to damage the corneal epithelium with a local anesthetic is similar to human pathology, in which a disturbance of the protective function of the corneal epithelium also facilitates infection by herpes simplex virus as well. The changes described are a starting point for further investigations.

Animals↗
PubMed2001

A germ-line Tsc1 mutation causes tumor development and embryonic lethality that are similar, but not identical to, those caused by Tsc2 mutation in mice.

Tuberous sclerosis (TS) is characterized by the development of hamartomas in various organs and is caused by a germ-line mutation in either TSC1 or TSC2 tumor suppressor genes. From the symptomatic resemblance among TS patients, involvement of TSC1 and TSC2 products in a common pathway has been suggested. Here, to analyze the function of the Tsc1 product, we established a line of Tsc1 (TSC1 homologue) knockout mouse by gene targeting. Heterozygous Tsc1 mutant (Tsc1(+/-)) mice developed renal and extra-renal tumors such as hepatic hemangiomas. In these tumors, loss of wild-type Tsc1 allele was observed. Homozygous Tsc1 mutants died around embryonic days 10.5-11.5, frequently associated with neural tube unclosure. As a whole, phenotypes of Tsc1 knockout mice resembled those of Tsc2 knockout mice previously reported, suggesting that the presumptive common pathway for Tsc1 and Tsc2 products may also exist in mice. Notably, however, development of renal tumors in Tsc1(+/-) mice was apparently slower than that in Tsc2(+/-) mice. The Tsc1 knockout mouse described here will be a useful model to elucidate the function of Tsc1 and Tsc2 products as well as pathogenesis of TS.

Animals↗