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PubMed1994

Clinical characteristics of illness caused by Bordetella parapertussis compared with illness caused by Bordetella pertussis.

In conjunction with a pertussis vaccine efficacy trial in Germany, nasopharyngeal specimens were collected from May, 1992, to March, 1993, from patients with cough illnesses. Clinical data were obtained by initial and follow-up questionnaires. Bordetella parapertussis was isolated from 38 patients (mean age, 3.5 years; 68% girls). Clinical characteristics in these cases were compared with those of 76 patients (matched by age and sex) with illness caused by Bordetella pertussis during the same period. Findings were: (B. pertussis/B. parapertussis): cough > 4 weeks 57%/37% (P = 0.06); whoop 80%/59% (P = 0.07); whoop > 2 weeks 26%/18% (P = 0.05); paroxysms 90%/83% (P = 0.5); body temperature > or = 38 degrees C 9%/0% (P = 0.17); vomiting 47%/42% (P = 0.69); and mean leukocyte and lymphocyte counts 12,500/mm3 and 7600/mm3 (P < 0.0001) and 7800/mm3 and 3500/mm3 (P < 0.0001), respectively. Illness caused by B. parapertussis was typical of pertussis but less severe than that caused by B. pertussis. In contrast with B. pertussis infection, lymphocytosis is not a characteristic of B. parapertussis infection. This is most likely a result of the lack of production of lymphocytosis-promoting factor toxin by B. parapertussis.

Bordetella↗
PubMed2005

Biceps tendinitis caused by an osteochondroma in the bicipital groove: a rare cause of shoulder pain in a baseball player.

Tendinitis of the long head of the biceps brachii muscle is commonly seen in athletes who do repetitive overhead motions. Common causes of biceps tendinitis include impingement syndrome, subluxation of the biceps tendon, and attrition tendinitis, whereas biceps tendinitis secondary to a bone neoplasm is rare. A case of biceps tendinitis caused by an osteochondroma arising in the left humeral bicipital groove in a 25-year-old male baseball player is reported. The tumor was hook-shaped, originated from the inferomedial portion of the humeral lesser tubercle, and surrounded the biceps tendon. Symptoms of increasing pain and inability to throw resulted from direct irritation of the biceps tendon by the tumor. Total excision of the tumor relieved the symptoms within 3 weeks. To our knowledge, there have been no reported cases in the English-language literature of biceps tendinitis caused by an osteochondroma.

Adult↗
PubMed2003

Can acute otitis media caused by Haemophilus influenzae be distinguished from that caused by Streptococcus pneumoniae?

BACKGROUND: Previous limited data suggest that acute otitis media (AOM) caused by Streptococcus pneumoniae can present as a more severe disease than that caused by Haemophilus influenzae or Moraxella catarrhalis, as expressed by both tympanic membrane and systemic findings. OBJECTIVES: To evaluate the severity of disease and impact of various pathogens, age, disease history and previous antibiotic therapy in children with AOM by using a comprehensive clinical/otologic score. PATIENTS AND METHODS: The study group consisted of 372 children ages 3 to 36 months with AOM seen at the pediatric emergency room during 1996 through 2001. All patients had tympanocentesis and middle ear fluid culture performed at enrollment. Clinical status was determined by a clinical/otologic score evaluating severity (0 = absent to 3 = severe) of tympanic membrane findings (redness and bulging) and patient's fever, irritability and ear tugging. Maximal severity score was 15. RESULTS: There were 138 (37%) H. influenzae, 76 (21%) S. pneumoniae, 64 (17%) mixed infections (H. influenzae + S. pneumoniae) and 94 (25%) culture-negative cases. The overall clinical/otologic score was higher in culture-positive than in culture-negative patients (9.27 +/- 2.75 vs.8.38 +/- 3.08, P = 0.01). When analyzed by age groups, this difference was significant only for the youngest age group (3 to 6 months, P = 0.05). The severity scores for AOM caused by H. influenzae and S. pneumoniae were significantly higher than in the culture-negative AOM when tympanic membrane redness and bulging were analyzed separately. No differences were recorded in clinical/otologic scores between different pathogens (9.49 +/- 2.86, 9.03 +/- 2.72 and 9.09 +/- 2.54 for H. influenzae, S. pneumoniae and H. influenzae + S. pneumoniae, respectively). The mean clinical/otologic score was higher in culture-positive than in culture-negative patients without relationship to previous antibiotic treatment or number of previous AOM episodes. CONCLUSIONS: (1) The clinical/otologic score of culture-positive young infants was higher than that of culture-negative infants; (2) the severity of tympanic membrane redness and bulging were the most indicative factors discriminating between a bacterial and nonbacterial etiology of AOM; and (3) the use of a clinical/otologic score could not discriminate among various bacterial etiologies of AOM.

Acute Disease↗
PubMed1981

An unusual cause of pacemaker current leakage causing muscle stimulation.

Stimulation of skeletal muscle is a fairly common complication of permanent cardiac pacing. The usual cause is direct apposition of the anode of a unipolar pacemaker with muscle surrounding the pocket. Other causes include electrode insulation defects and electrode displacement. In this report we describe an unusual cause of muscle stimulation related to direct current leakage from the pacemaker.

Aged↗
PubMed1997

Perimetric probability maps to separate change caused by glaucoma from that caused by cataract.

We describe a new method for analysis of change in glaucomatous visual fields with the object to differentiate between changes caused by glaucoma from those caused by cataract. New pattern deviation change probability maps were developed from a prospectively collected glaucoma material and designed to be sensitive to changes in localized field loss, but to be unaffected by media-induced perimetric change. We compared the new change probability maps with the commercially available total deviation change probability maps in series of Humphrey perimetric tests in a glaucoma material of 43 eyes of 35 patients, who had undergone cataract surgery. When using the total deviation maps, considerable differences were seen between fields obtained before and after cataract surgery. Much smaller differences were seen when using the new change probability maps, that almost eliminated the common and disturbing effect of increasing cataract. This new tool could be of considerable help in differentiation between progressive glaucomatous visual field loss and deterioration caused by increasing media opacities.

Aged↗
PubMed2004

Valproic acid is known to cause hypospadias in man but does not reduce anogenital distance or causes hypospadias in rats.

The use of valproic acid during human pregnancy increases the risk of hypospadias in the offspring. Rats exposed in utero to valproic acid did not develop hypospadias and even had a slightly increased anogenital distance in males 3-4 days after birth. A classical antiandrogenic drug, flutamide, caused hypospadias as well as a reduction of the anogenital distance in males. At the age of 3 months, rats exposed in utero with either valproic acid or flutamide showed a reduced testicular weight and hypoplasia of tubules, which seemed not to be related to the antiandrogenic activity of flutamide as it did not correlate with the presence of hypospadias. The mechanism through which valproic acid causes hypospadias in man and affects testicular development in rat is unknown. Hypospadias caused by valproic acid in man is apparently not due to anti-androgenic properties of the drug.

Androgen Antagonists↗
PubMed2003

Cryptococcus neoformans with a mutation in the tetratricopeptide repeat-containing gene, CCN1, causes subcutaneous lesions but fails to cause systemic infection.

We studied a Cryptococcus neoformans strain that caused feline chronic nasal granuloma without disseminated disease. This strain, B-4551, grows at temperatures up to 35 degrees C and fails to cause systemic infection in mice. Many cells of B-4551 formed short hyphal elements in feline nasal tissue and occasionally at 35 degrees C in vitro. A complementation and sequence analysis revealed that the temperature-sensitive (Ts) phenotype of B-4551 was due to deletion of a lysine residue in the cryptococcal CCN1 gene. B-4551 complemented with the wild type CCN1 gene grew at 37 degrees C and caused fatal systemic infection in mice. The CCN1 gene encodes a protein containing 16 copies of a tetratricopeptide repeat. CCN1 is homologous to the Saccharomyces cerevisiae CLF1 gene, which is required for pre-mRNA splicing, cell cycle progression, and DNA replication, and to the Drosophila melanogaster crn gene, which is involved in neurogenesis. CLF1 complemented the Ts phenotype of B-4551. CCN1, however, failed to rescue the clf1 mutant in S. cerevisiae. These results indicate that the Ccn1p may not be as functionally diverse as Clf1p in yeast.

Amino Acid Sequence↗
PubMed1996

Acute intermittent porphyria caused by defective splicing of porphobilinogen deaminase RNA: a synonymous codon mutation at -22 bp from the 5' splice site causes skipping of exon 3.

Acute intermittent porphyria (AIP) results from mutations in the porphobilinogen deaminase (PBG) gene. Three of 14 randomly selected, unrelated patients with the cross reacting immunological material (CRIM) negative form of AIP were found to have previously undescribed RNA splicing defects. Defective splicing of exons 12 and 13 was caused by a C-->G transversion at position -3 of the 3' splice site of intron 11 and a G-->A transition at the first position of intron 13, respectively. Defective splicing of exon 3 was associated with a synonymous codon mutation (CGC-->CGG, R28R) at position -22 from the 5' splice site. Our findings are consistent with previous reports indicating that about 15% of mutations in the PBG deaminase gene that cause AIP affect RNA splicing and add to the evidence that synonymous intraexonic codon mutations may cause disease.

Acute Disease↗
PubMed2005

Mineralocorticoid receptor activation causes cerebral vessel remodeling and exacerbates the damage caused by cerebral ischemia.

Mineralocorticoid receptor antagonists protect against ischemic cerebrovascular disease; this appears to be caused by changes in cerebral vessel structure that would promote blood flow. Therefore, we hypothesized that mineralocorticoid receptor activation with deoxycorticosterone acetate would cause deleterious remodeling of the cerebral vasculature and exacerbate the damage caused by cerebral ischemia. Six-week-old male Wistar rats were treated with deoxycorticosterone acetate (200 mg/kg) for 6 weeks. At 12 weeks of age, the deoxycorticosterone acetate-treated rats had elevated systolic blood pressure compared with age-matched controls (157+/-5.9 versus 124+/-3.1 mm Hg deoxycorticosterone acetate versus control; P<0.05). The area of ischemic damage resulting from middle cerebral artery occlusion was greater in the deoxycorticosterone acetate-treated rats than control (63.5+/-3.72 versus 46.6+/-5.52% of the hemisphere infarcted, deoxycorticosterone acetate versus control; P<0.05). Middle cerebral artery structure was assessed using a pressurized arteriograph under calcium-free conditions. Over a range of intralumenal pressures, the lumen and ODs of the middle cerebral arteries were smaller in the deoxycorticosterone acetate-treated rats than the control rats (P<0.05). There was also an increase in the wall thickness and wall:lumen ratio in the vessels from deoxycorticosterone acetate-treated rats (P<0.05). The vessels from the deoxycorticosterone acetate-treated rats were stiffer than those from control rats as evidenced by a leftward shift in the stress/strain curve. These novel data suggest that mineralocorticoid receptor activation without salt loading and nephrectomy is sufficient to elicit deleterious effects on the cerebral vasculature that lead to inward hypertrophic remodeling and an increase in the ischemic damage in the event of a stroke.

Animals↗
PubMed1995

Somatic mutations causing constitutive activity of the thyrotropin receptor are the major cause of hyperfunctioning thyroid adenomas: identification of additional mutations activating both the cyclic adenosine 3',5'-monophosphate and inositol phosphate-Ca2+ cascades.

A series of somatic mutations of the TSH receptor gene have been demonstrated in hyperfunctioning thyroid adenomas. The mutations studied up to now cause constitutive (i.e. TSH-independent) activation of the cAMP-regulatory cascade only. As a follow-up to our original study, we have now completely sequenced exon number 10 of the TSH receptor gene in the same series of toxic adenomas. An activating mutation was found in nine of 11 tumors. In addition to the mutations already described, two isoleucine residues belonging to the first and second extracellular loops of the receptor (Ile486 and Ile568) were found mutated. Two different adenomas were found to harbor a different amino acid substitution at residue 486 (Ile486Phe, Ile486Met). Ile568 was mutated to threonine in one. When studied by transfection in COS-7 cells, all three mutations caused very strong activation of the cAMP-regulatory cascade. In addition, the Ile486Phe and, to a lesser extent, the Ile486Met and Ile568Thr mutants stimulated constitutively the inositol phosphate-diacylglycerol cascade. Our results demonstrate that 1) the first and second extracellular loops contribute to the silencing of the unliganded TSH receptor; 2) the two regulatory cascades normally under TSH control can be constitutively activated by somatic mutations of the receptor; 3) the TSH receptor can be activated by mutation of a large number of residues distributed over the first and second extracellular loops, the third intracellular loop, and the third, sixth, and seventh transmembrane segments; 4) activating mutations of the TSH receptor constitute the major cause of toxic adenomas, accounting for about 80% of the cases.

Adenoma↗
PubMed2005

Spontaneous fractures in the mouse mutant sfx are caused by deletion of the gulonolactone oxidase gene, causing vitamin C deficiency.

UNLABELLED: Using a mouse mutant that fractures spontaneously and dies at a very young age, we identified that a deletion of the GULO gene, which is involved in the synthesis of vitamin C, is the cause of impaired osteoblast differentiation, reduced bone formation, and development of spontaneous fractures. INTRODUCTION: A major public health problem worldwide, osteoporosis is a disease characterized by inadequate bone mass necessary for mechanical support, resulting in bone fracture. To identify the genetic basis for osteoporotic fractures, we used a mouse model that develops spontaneous fractures (sfx) at a very early age. MATERIALS AND METHODS: Skeletal phenotype of the sfx phenotype was evaluated by DXA using PIXImus instrumentation and by dynamic histomorphometry. The sfx gene was identified using various molecular genetic approaches, including fine mapping and sequencing of candidate genes, whole genome microarray, and PCR amplification of candidate genes using cDNA and genomic DNA as templates. Gene expression of selected candidate genes was performed using real-time PCR analysis. Osteoblast differentiation was measured by bone marrow stromal cell nodule assay. RESULTS: Femur and tibial BMD were reduced by 27% and 36%, respectively, in sfx mice at 5 weeks of age. Histomorphometric analyses of bones from sfx mice revealed that bone formation rate is reduced by >90% and is caused by impairment of differentiated functions of osteoblasts. The sfx gene was fine mapped to a 2 MB region containing approximately 30 genes in chromosome 14. By using various molecular genetic approaches, we identified that deletion of the gulonolactone oxidase (GULO) gene, which is involved in the synthesis of ascorbic acid, is responsible for the sfx phenotype. We established that ascorbic acid deficiency caused by deletion of the GULO gene (38,146-bp region) contributes to fractures and premature death because the sfx phenotype can be corrected in vivo by treating sfx mice with ascorbic acid and because osteoblasts derived from sfx mice are only able to form mineralized nodules when treated with ascorbic acid. Treatment of bone marrow stromal cells derived from sfx/sfx mice in vitro with ascorbic acid increased expression levels of type I collagen, alkaline phosphatase, and osteocalcin several-fold. CONCLUSION: The sfx is a mutation of the GULO gene, which leads to ascorbic acid deficiency, impaired osteoblast cell function, and fractures in affected mice. Based on these and other findings, we propose that ascorbic acid is essential for the maintenance of differentiated functions of osteoblasts and other cell types.

Animals↗
PubMed2007

Aggregated myocilin induces russell bodies and causes apoptosis: implications for the pathogenesis of myocilin-caused primary open-angle glaucoma.

Primary open-angle glaucoma with elevated intraocular pressure is a leading cause of blindness worldwide. Mutations of myocilin are known to play a critical role in the manifestation of the disease. Misfolded mutant myocilin forms secretion-incompetent intracellular aggregates. The block of myocilin secretion was proposed to alter the extracellular matrix environment of the trabecular meshwork, with subsequent impediment of aqueous humor outflow leading to elevated intraocular pressure. However, the molecular pathogenesis of myocilin-caused glaucoma is poorly defined. In this study, we show that heteromeric complexes composed of wild-type and mutant myocilin were retained in the rough endoplasmic reticulum, aggregating to form inclusion bodies typical of Russell bodies. The presence of myocilin aggregates induced the unfolded protein response proteins BiP and phosphorylated endoplasmic reticulum-localized eukaryotic initiation factor-2alpha kinase (PERK) with the subsequent activation of caspases 12 and 3 and expression of C/EBP homologous protein (CHOP)/GADD153, leading to apoptosis. Our findings identify endoplasmic reticulum stress-induced apoptosis as a pathway to explain the reduction of trabecular meshwork cells in patients with myocilin-caused glaucoma. As a consequence, the phagocytotic capacity of the remaining trabecular meshwork cell population would be insufficient for effective cleaning of aqueous humor, constituting a major pathogenetic factor for the development of increased intraocular pressure in primary open-angle glaucoma.

Animals↗
PubMed1993

Judging interevent relations: from cause to effect and from effect to cause.

Stimulus competition was studied in college students' correlational judgments in a medical decision-making setting. In accord with prior findings, subjects making cause-to-effect (predictive) judgments discounted a stimulus event that was moderately correlated with a target event when rival stimuli were more highly correlated with the effect. However, subjects making effect-to-cause (diagnostic) judgments were not at all disposed to discount a stimulus event which was moderately correlated with a target event when rival stimuli were more highly correlated with the cause. The theoretical implications of these results are considered in connection with associative and mentalistic models of causal attribution.

Adolescent↗
PubMed1993

Glycine protects hepatocytes from injury caused by anoxia, cold ischemia and mitochondrial inhibitors, but not injury caused by calcium ionophores or oxidative stress.

Isolated hepatocytes, suspended in an organ preservation solution, can be preserved at 4 degrees C for up to 6 days. After preservation, normothermic-normoxic incubation causes loss of hepatocyte viability. The addition of 3 mmol/L glycine to the rewarming medium prevents the loss of viability. In this study we investigated the cytoprotective effects of glycine under many conditions known to cause hepatocellular injury to understand the mechanism of cold-induced injury in the liver. Hepatocytes were suspended in modified Krebs-Henseleit buffer with or without 3 mmol/L glycine and exposed to agents or conditions known to induce cell death. Hepatocyte viability was assessed by measuring the percentage of lactate dehydrogenase leakage from the cells and the concentration of ATP during incubation at 37 degrees C under room air for up to 90 min. Mitochondrial inhibitors (potassium cyanide and carbonyl cyanide m-chlorophenylhydrazone); calcium ionophores (ionomycin and A23187); an oxidizing agent, tert-butyl hydroperoxide; and anoxia were all used to cause cell injury. Hepatocytes were also isolated from fasted rats and hypothermically preserved as another model of cell death. Other amino acids were also tested in the hypothermic preservation model to study the specificity of the amino acid requirement for prevention of lactate dehydrogenase leakage. Of the amino acids tested, only alanine (10 mmol/L) and the combination of alanine (3 mmol/L) and serine (3 mmol/L) were as effective as glycine in preventing lactate dehydrogenase release in the hypothermic preservation model.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids↗
PubMed2001

Socioeconomic inequalities in all-cause and specific-cause mortality in Australia: 1985-1987 and 1995-1997.

BACKGROUND: Socioeconomic inequalities in mortality have been repeatedly observed in Britain, the US, and Europe, and in some countries there is evidence that the differentials are widening. This study describes trends in socioeconomic mortality inequality in Australia for males and females aged 0-14, 15-24 and 25-64 years over the period 1985-1987 to 1995-1997. METHODS: Socioeconomic status (SES) was operationalized using the Index of Relative Socioeconomic Disadvantage, an area-based measure developed by the Australian Bureau of Statistics. Mortality differentials were examined using age-standardized rates, and mortality inequality was assessed using rate ratios, gini coefficients, and a measure of excess mortality. RESULTS: For both periods, and for each sex/age subgroup, death rates were highest in the most disadvantaged areas. The extent and nature of socioeconomic mortality inequality differed for males and females and for each age group: both increases and decreases in mortality inequality were observed, and for some causes, the degree of inequality remained unchanged. If it were possible to reduce death rates among the SES areas to a level equivalent to that of the least disadvantaged area, premature all-cause mortality for males in each age group would be lower by 22%, 28% and 26% respectively, and for females, 35%, 70% and 56%. CONCLUSIONS: The mortality burden in the Australian population attributable to socioeconomic inequality is large, and has profound and far-reaching implications in terms of the unnecessary loss of life, the loss of potentially economically productive members of society, and increased costs for the health care system.

Adolescent↗
PubMedDate not supplied

[Reliability of information on the underlying cause of death from external causes in people under 18 years of age in the Municipality of Duque de Caxias, Rio de Janeiro, Brazil].

This study assesses the quality of official data on mortality due to external causes. It examines the agreement in the underlying cause of death by accidents and violence in children and adolescents under 18 years of age in the Municipality of Duque de Caxias, Rio de Janeiro State. Codings based on death certificates (DC) issued by the Institute of Forensic Medicine - IFM (ICDifm) and those complemented by the Municipal Secretariat of Health - MSH (ICDmsh) are compared to the coding directly obtained from autopsy logs and attached to police reports accessible at the IFM (ICDresearch). Levels of agreement (kappa) between ICDmsh/ICDifm, ICDresearch/ ICDifm, and ICDresearch/ICDmsh were 0.33, 0.26, and 0.81, respectively, in 1995 and 0.26, 0.22, and 0.71 in 1996. When analyzed together, all three sources agreed by 45% and 37.6% in the respective years. ICDresearch and ICDmsh agreed among themselves and disagreed with ICDifm by 46.9% in 1995 and 48.2% in 1996. Results show that the IFM fails to transfer available information to the MSH via DCs. Although a satisfactory updating is subsequently carried out at the MSH, the relevance and legality of this procedure should be called into question and further discussed.

Accidents↗
PubMed2004

All-cause and cause-specific mortality by socioeconomic status among employed persons in 27 US states, 1984-1997.

OBJECTIVES: We investigated mortality differences according to socioeconomic status (SES) for employed persons in 27 states during 1984-1997. METHODS: SES was determined for persons aged 35-64 years according to the "usual occupation" listed on their death certificates. We used US Census denominator data. RESULTS: For all-cause mortality, rate ratios from lowest to highest SES quartile for men and women were 2.02, 1.69, 1.25, and 1.00 and 1.29, 1.01, 1.07, and 1.00, respectively. Percentage of all deaths attributable to being in the lowest 3 SES quartiles was 27%. Inverse SES gradients were strong for most major causes of death except breast cancer and colorectal cancer. Heart disease mortality for highest and lowest SES quartiles dropped 45% and 25%, respectively, between 1984 and 1997. CONCLUSIONS: Mortality differences by SES were sustained through the 1990s and are increasing for men.

Adult↗
PubMed1996

Breast cancer as cause of death--a study over the validity of the officially registered cause of death in 2631 breast cancer patients dying in Malmö, Sweden 1964-1992.

The validity of registered official cause of death (COD) concerning breast cancer patients in Malmö 1964-1992 was analysed. There was a high frequency of autopsy in the material and, therefore, the number of diagnostic errors should be low. Found discordance thus mostly reflect the quality of certifying and registration of COD. Of 2631 deaths discordance was found as to underlying COD in 121 cases (4.6%). Ninety-four of these represent outright errors. In 27 there was doubt about the reported COD. The number of discordant cases increased with age at death. Two kinds of systematic bias were found. One was a tendency to report breast cancer as contributing COD in patients with clinical cure. The other was a practice at the Registry to register breast cancer as underlying COD in cases with breast cancer reported as contributing COD. This practice was changed in 1981 causing an artificial decrease in registered breast cancer mortality.

Breast Neoplasms↗