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PubMed1989

Retrograde intrabiliary injection of amphipathic materials causes phospholipid secretion into bile. Taurocholate causes phosphatidylcholine secretion, 3-[(3-cholamidopropyl)dimethylammonio]-propane-1-sulphonate (CHAPS) causes mixed phospholipid secretion.

The control of biliary phospholipid and cholesterol secretions by bile acid was studied by using the technique of retrograde intrabiliary injection. Taurocholate (TC), a moderately hydrophobic bile acid, taurodehydrocholate (TDHC), a hydrophilic non-micelle-forming bile acid, and 3-[(3-cholamidopropyl)-dimethylammonio]propane-1-sulphonate (CHAPS), a detergent, were individually administered by retrograde intrabiliary injection (RII) into the biliary tree, and bile acids, phospholipids and cholesterol subsequently appearing in the bile were measured. TC (1.3 mumol; 45 microliters) injected retrogradely provoked a 3.5-fold increase in biliary phospholipid output for 40 min, as compared with the saline control. Injection of 2.7 mumol of TC (90 microliters) caused a 7.5-fold increase in phospholipid output, which reached a peak at 12 min after RII, and phospholipid output continued for 40 min. Cholesterol output was also elicited under these conditions, showing both dose-dependency and extended secretion. Injection of 1.8 mumol of TDHC caused very little increase in either biliary phospholipid or cholesterol. Injection of 0.9 mumol of CHAPS (45 microliters) provoked a single substantial peak of phospholipid output in the 3 min bile sample. T.l.c. analysis of the phospholipid extracts of the bile collected after each compound showed, for TC, a single compound which co-migrated with the phosphatidylcholine standard, whereas for CHAPS substantial amounts of other phospholipids were present.

Animals↗

PubMed1989

H-7, a protein kinase C inhibitor, inhibits phorbol ester-caused ornithine decarboxylase induction but fails to inhibit phorbol ester-caused suppression of epidermal growth factor binding in primary cultured mouse epidermal cells.

12-O-tetradecanoylphorbol-13-acetate (TPA) induced ornithine decarboxylase (ODC) and suppressed 125I-epidermal growth factor (EGF) binding in primary cultured mouse epidermal cells. TPA (30 nM)-caused ODC induction was almost completely blocked by 30 microM H-7 [1-(5-isoquinolinylsulfonyl)-2-methylpiperazine], a well known protein kinase C inhibitor, but the same concentration of H-7 failed to restore the 125I-EGF binding suppressed by TPA (10 nM). On the other hand, sphingosine, another protein kinase C inhibitor, blocked not only TPA-caused ODC induction but also TPA-caused suppression of 125I-EGF binding. Concentration-response curves of sphingosine for these two TPA-caused cellular responses were almost identical. 1,2-Diacylglycerols such as 1,2-dioctanoylglycerol (30-300 microM) and 1-oleoyl-2-acetylglycerol (OAG) (30-300 microM) mimicked TPA actions. Similar to the case of TPA, suppression of 125I-EGF binding by OAG was barely inhibited by H-7, whereas sphingosine was more effective in inhibiting the OAG-caused suppression of 125I-EGF binding than was H-7. In TPA (50 nM)-pretreated epidermal cells, TPA (10 nM) failed to suppress 125I-EGF binding. H-7 (30 microM) did not affect TPA (30 nM)-caused translocation of protein kinase C. These results clearly demonstrate the differential inhibition by H-7 of the TPA-caused cellular responses and indicate that TPA-caused suppression of 125I-EGF binding to epidermal cells is mediated through protein kinase C function, which is barely inhibited by H-7.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed1979

Effects of dependency among causes of death for cause elimination life table strategies.

A study is made of the effects of associated causes of death, and of dependency among causes of death, by observing the relative importance of one cause of death when another is eliminated under various competing risk models. Two disease pairs, cancer and infectious disease and stroke and ischemic heart disease, are selected for analysis because they represent different types of disease dependence. Crude probabilities of death for each disease are calculated for the U.S. white male population in 1969. Next, the effects of the complementary disease in a pair are hypothetically eliminated in one of three ways: (a) a standard competing risk adjustment for cause elimination when deaths are singly caused (Chiang, 1968), (b) lethal defect-pattern of failure computations for multiply caused death when no causal order is inferred (Manton et al., 1976), and (c) relative susceptibility, computations for multiply caused deaths when causes are ordered (Wong, 1977). The paper closes with a discussion of the relative merits of the three types of adjustments.

Actuarial Analysis↗

PubMed2024

Long-term exposure to particulate matter and all-cause and cause-specific mortality in an analysis of multiple Asian cohorts.

BACKGROUND: Exposure to ambient air pollution is associated with a significant number of deaths. Much of the evidence associating air pollution with adverse effects is from North American and Europe, partially due to incomplete data in other regions limiting location specific examinations. The aim of the current paper is to leverage satellite derived air quality data to examine the relationship between ambient particulate matter and all-cause and cause-specific mortality in Asia. METHODS: Six cohorts from the Asia Cohort Consortium provided residential information for participants, recruited between 1991 and 2008, across six countries (Bangladesh, India, Iran, Japan, South Korea, and Taiwan). Ambient particulate material (PM2·5) levels for the year of enrolment (or 1998 if enrolled earlier) were assigned utilizing satellite and sensor-based maps. Cox proportional models were used to examine the association between ambient air pollution and all-cause and cause-specific mortality (all cancer, lung cancer, cardiovascular and lung disease). Models were additionally adjusted for urbanicity (representing urban and built characteristics) and stratified by smoking status in secondary analyses. Country-specific findings were pooled via random-effects meta-analysis. FINDINGS: More than 300,000 participants across six cohorts were included, representing more than 4-million-person years. A positive relationship was observed between a 5 µg/m (Dockery et al., 1993) increase in PM2·5 and cardiovascular mortality (HR: 1·06, 95 % CI: 0.99, 1·13). The additional adjustment for urbanicity resulted in increased associations between PM2.5 and mortality outcomes, including all-cause mortality (1·04, 95 % CI: 0·97, 1·11). Results were generally similar regardless of whether one was a current, never, or ex-smoker. INTERPRETATION: Using satellite and remote sensing technology we showed that associations between PM2.5 and all-cause and cause-specific Hazard Ratios estimated are similar to those reported for U.S. and European cohorts. FUNDING: This project was supported by the Health Effects Institute. Grant number #4963-RFA/18-5. Specific funding support for individual cohorts is described in the Acknowledgements.

Humans↗

PubMed1987

On the use of the cause table in handling common cause events in system analysis.

A method is presented for applying the cause table concept to the problem of common cause events. This method can be regarded as an alternative to the approach in which these events are included directly into the system fault trees. In comparison with this approach, the cause table method offers the advantage of simple fault trees, convenient visibility of the contributions of causes, and the ability to truncate the numerical calculation conveniently by aggregating small terms into an "other" category. Generally speaking, the cause table method can be said to handle common causes at the level of arithmetic (i.e., numbers) rather than at the level of algebra (determining cutsets and frequency equations).

Methods↗

PubMedDate not supplied

Cerebral hemorrhagic infarction at autopsy: cardiac embolic cause and the relationship to the cause of death.

In 48 patients dying within 15 days following a supra-tentorial cerebral infarct, the presence of hemorrhagic infarction at autopsy was related to a cardiac embolic cause of the infarct, and to the cause of death. Hemorrhagic infarcts were more common among patients dying from brain herniation than among those dying from a non-cerebral cause. Cardiac embolic strokes were more often hemorrhagic at autopsy than strokes without such cause; this could be explained by a significant higher rate of brain herniation and death after embolic stroke. On the other hand infarcts with extended hemorrhages more often tended to have a cardiac than a non-cardiac cause. These data, together with earlier clinical findings suggest that autopsy studies are biased in relating hemorrhagic infarction almost exclusively to a cardiac embolic cause of stroke, although cardiac emboli may produce more extended hemorrhages.

Adult↗

PubMed1991

Causes of death in a cohort of 50,465 young men--validity of recorded suicide as underlying cause of death.

We studied causes of death in a cohort of all young males (n = 50,465) conscripted for military service in 1969-70. Six hundred eighty three deaths occurred in the cohort during the follow-up through 1983. Injury-related deaths accounted for 75% of all deaths. Of these, 38% were definite suicides, 10% undetermined suicides and 30% motor vehicle accidents. The validity of officially recorded causes of death was studied by scrutinizing all death certificates (n = 683) and forensic reports, including police reports, toxicological and histological data, from a sample (n = 322) of deaths with unclear circumstances. Of 161 officially recorded suicides (E950-959), only one case was reevaluated into poisoning, "undetermined" (E980). Of 47 cases officially recorded "undetermined" (E980-989), 9 were reevaluated into definite suicide (E950-959) although we believe that this is still an underestimation of "true" suicide cases. An alcohol concentration of more than 0.1 g% was found in 45% of all violent deaths (E800-999), 34% of all suicides and 60% of all "undetermined" deaths. We conclude that the causes of death in most cases of injury related death in young age are recorded with high accuracy. Reevaluation of recorded deaths from "undetermined" causes revealed a number of definite suicides, although the "true" number of suicides is difficult to assess even after close scrutiny of the information available.

Accidents↗

PubMed2025

High-fat and low-fat fermented milk and cheese intake, proteomic signatures, and risk of all-cause and cause-specific mortality.

PURPOSE: This study aimed to examine the associations between the intake of high- and low-fat fermented dairy (cheese and fermented milk), their proteomic profiles, and mortality risk. METHODS: This cohort study included 25,187 participants (mean age 57.7 years, 60.9% females). Fermented dairy intake was assessed by a modified diet history method. In a random subset of this cohort (n = 4359), we constructed proteomic signatures for fermented dairy intake using 136 candidate plasma proteins. RESULTS: During 23.5 years of follow-up, 9742 participants died. High-fat cheese (> 20% fat) intake was inversely associated with risk of all-cause mortality (HR for an increment of 20 g/day, 0.97; 95% CI, 0.96-0.99, P < 0.001) and cardiovascular disease mortality (HR, 0.96; 95% CI, 0.93-0.99, P = 0.006). Low-fat cheese intake showed an inverse association with all-cause mortality (HR, 0.98; 95% CI, 0.96-1.00, P = 0.047). Low-fat fermented milk intake was inversely associated with all-cause mortality (HR for an increment of 250 g/day, 0.91; 95% CI, 0.85-0.97, P = 0.006), while high-fat fermented milk (> 2.5% fat) showed null association. A total of 42, 26, 0, and 39 proteins were identified for the signature of high-fat cheese, low-fat cheese, high-fat fermented milk, and low-fat fermented milk, respectively. Inverse associations with all-cause mortality were observed for all three signatures with identified proteins. The identified proteins were involved in biological pathways related to immune response and inflammation. CONCLUSION: Our study indicated that consuming high-fat cheese, low-fat cheese, and low-fat fermented milk was linked to survival benefits. Plasma proteins improve our understanding of the health effects of fermented dairy.

Humans↗

PubMed1991

v-abl causes hematopoietic disease distinct from that caused by bcr-abl.

v-abl, the oncogene transduced by Abelson murine leukemia virus, was first characterized by its ability to transform lymphoid cells. bcr-abl, the oncogene formed by a t(9;22) translocation thought to occur in human hematopoietic stem cells, is detectable in almost all cases of chronic myelogenous leukemia (CML), a malignancy of granulocytic cells. bcr-abl also causes a CML-like syndrome in mice whose bone-marrow cells are infected with a retrovirus transducing the gene. More recent reports have suggested that v-abl can, however, cause a disease similar to CML. We demonstrate here that v-abl, when transduced in a helper virus-containing system, causes disease similar to, but distinct from, the CML-like syndrome induced by bcr-abl. Animals whose bone marrow has been infected by v-abl virus develop modest splenomegaly, marked granulocytosis, and malignant disease of several hematopoietic cell types. Unlike animals with CML-like disease resulting from bcr-abl, the polymorphonuclear leukocytes from animals infected with a v-abl construct do not contain the v-abl provirus at a significant frequency. Histopathologic analysis also shows significant differences between the diseases caused by v-abl and bcr-abl.

Abelson murine leukemia virus↗

PubMed1992

[A case of chronic persistent cough (CPC) caused by gastroesophageal reflux (GER) (including a study of CPC caused by suspected GER)].

A patient, an 80-year-old female, had complained of a cough for 20 weeks, and was not cured by cough medicine. Gastroesophageal reflux was considered as the cause of the cough because of her symptoms and gastrointestinal fiberscopy (GIF) and barium meal studies. She made favorable progress on a histamine H2 blocker and cysapurid for 4 weeks. Therefore we diagnosed her cough as caused by gastroesophageal reflux. We also studied the incidence of chronic persistent cough in patients suspected of gastroesophageal reflux because of symptoms and GIF results. Among 676 cases examined by GIF at Niigata-kenritsu Myoko Hospital, we detected 7 cases who complained of heartburn and in whom we observed hiatal hernia and reflux esophagitis by GIF. Only one of them, the present case, complained of a cough. CPC caused by gastroesophageal reflux is not seen frequently, but the possibility of GER as the cause of CPC should be considered.

Aged↗

PubMed1986

[Morbidity status, causes for work disability and social factors influencing work disability in pregnancy. 2. Causes for work disability].

The higher level of patients of pregnant woman in comparison with non-pregnant ones results from a higher unfitness for work which nearly corresponds to the increase of sicknesses depending on gestation. From all causes of unfitness for work more than 60% were depending on gestation. Causes for the half of the release from work depending on gestation were the three diagnoses threatening abortion, threatening premature birth and bleedings. On the total level of patients of 11.66% they had a share of 5.70% points. Infections of the ureter, the diagnosis' 'Other complications in pregnancy', hyperemesis and gestoses followed. Infections of the upper respiratory tract and influenza were the causes of all releases from work which were not depending on gestation. Their share on the level of patients amounted to 0.9% points. Releases from work because of sicknesses of circulation and of the digestive tract followed in their frequency. A number of further causes of unfitness for work had only a small share on the happenings of unfitness for work.

Abortion, Spontaneous↗

PubMed1989

Significant changes in nonspecific bronchial responsiveness after isolated immediate bronchospecific reactions caused by isocyanates but not after a late reaction caused by plicatic acid.

Although late bronchospastic reactions after exposure to antigenic and sensitizing agents usually significantly alter bronchial responsiveness to histamine or methacholine, presumably by causing bronchial inflammation, isolated immediate bronchospastic reactions do not induce such changes. We studied three subjects who demonstrated different patterns of reaction. The first individual was diagnosed as having occupational asthma to red cedar. This was confirmed by specific inhalation challenges that resulted in late bronchospastic reaction. No significant changes in the provocative concentration of histamine causing a 20% fall in FEV1 (PC20) were found 1 day after this reaction. Two weeks later, serial assessments (five and six, respectively) of PC20 histamine were recorded on control days and up to 48 hours after exposure to plicatic acid, which caused a late bronchospastic reaction with a maximum fall of 37% in FEV1. No significant changes in PC20 were found; the maximum variations on control days were 0.36 to 0.74 mg/ml, and on active days, from 0.37 to 0.59 mg/ml. By contrast, two other subjects, who demonstrated isolated immediate reactions after exposure to diphenylmethane diisocyanate, had significant changes in PC20 histamine and methacholine, in one subject from 3.1 mg/ml to 0.6 mg/ml 8 hours after exposure, and in the other subject, from 61.0 to 7.4 mg/ml 7 hours after exposure, with recovery during the next few days. These examples demonstrate that the pattern of nonspecific bronchial responsiveness after immediate and late bronchospastic reactions can be different from what has previously been described. Immediate bronchospastic reactions may lead to bronchial hyperresponsiveness, whereas late asthmatic reactions do not always induce changes in bronchial responsiveness.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

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↗

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↗

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↗

PubMed1992

[Apropos of a rare cause of torsades de pointe: hypokalemia caused by dietary deficiency].

The authors report a case of wave burst arrhythmia in a young immigrant woman of Laotian origin aged 32. The main cause of the arrhythmia was related to potassium deficiency of dietary origin. Some contributory factors may have had a promoting effect: theophylline treatment, beta-mimetics and adrenaline (epinephrine). This case can therefore be related to the cases of wave burst arrhythmia and hypokalemia previously reported in anorexic subjects. This case suggests that special attention should be paid to the diet of some ethnic groups who have been displaced by economic causes. Their very unusual dietary habits may induce or aggravate hypokalemia, which may also be promoted in some cases by drugs. Some treatments should therefore be introduced with caution in this context due to the potential risk of inducing severe arrhythmia.

Adult↗

PubMed1992

Case report of an unusual cause of low back pain. Intervertebral diskitis caused by Eikenella corrodens.

A 42-year-old man suffered from low back pain caused by intervertebral diskitis. The condition was diagnosed on plain roentgenogram and computed tomography scans. The infected area was biopsied and grew Eikenella corrodens, a gram-negative anaerobic rod, which grows slowly only after culture on blood agar in 5-10% carbon dioxide. This is the first reported case of E. corrodens intervertebral diskitis causing acute low back pain. Recognition of this organism in this condition emphasizes the importance of aerobic and anaerobic cultures of infected disks. The organism has unusual antibiotic sensitivities. The infection, once appropriately treated, responded rapidly.

Adult↗