Turn complaints into assets with a physicians' complaint system.
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Biomedical subjects
Publications and source records attributed to J Jensen.
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We investigated the effects of insulin and adrenaline on the rate of glycogen synthesis in skeletal muscles after electrical stimulation in vitro. The contractile activity decreased the glycogen concentration by 62%. After contractile activity, the glycogen stores were fully replenished at a constant and high rate for 3 h when 10 m-i.u./ml insulin was present. In the absence of insulin, only 65% of the initial glycogen stores was replenished. Adrenaline decreased insulin-stimulated glycogen synthesis. Surprisingly, adrenaline did not inhibit glycogen synthesis stimulated by glycogen-depleting contractile activity. In agreement with this, the fractional activity of glycogen synthase was high when adrenaline was present after exercise, whereas adrenaline decreased the fractional activity of glycogen synthase to a low level during stimulation with insulin. Furthermore, adrenaline activated glycogen phosphorylase almost completely during stimulation with insulin, whereas a much lower activation of glycogen phosphorylase was observed after contractile activity. Thus adrenaline does not inhibit contraction-stimulated glycogen synthesis.
BACKGROUND: Structured feedback of information can produce change in physician behaviour. The objective of this study was to assess the effectiveness of 2 educational interventions for improving the quality of care provided by family physicians in Ontario: the Practice Assessment Report (PAR) and the Continuing Medical Education Plan (CMEP) with a follow-up visit by a mentor. METHODS: The study was a randomized controlled trial. Physicians in the control group received only the PAR, whereas those in the experimental group received the PAR, CMEP and mentor interventions. The participants were 56 family physicians and general practitioners (27 in the PAR group and 29 in the CMEP group) in southern Ontario who agreed to participate in the interventions and provide data. A total of 2395 patients randomly sampled from the practices returned questionnaires and consented to have their medical records abstracted. The outcome measures were global scores in 4 areas--quality of care, charting, prevention and overall use of medications--and patient ratings of satisfaction with care and preventive practices. The measures were applied at the beginning (phase 1) and end (phase 2) of the study. RESULTS: The mean global scores at the end of the study for the PAR group were 70.1% for quality of care, 84.7% for prevention, 77.7% for charting and 82.2% for overall use of medications. The corresponding scores for the CMEP group were 68.3%, 82.1%, 76.4% and 83.2%. In the patient satisfaction component, the personal care scores at phase 2 were 93.6% for the PAR group and 94.6% for the CMEP group. Examples of the scores for prevention for the PAR group were 98.3% for children's current immunization, 96.6% for blood pressure measured within the previous 5 years, 79.4% for referral of women of the appropriate age for mammography within the previous 2 years, and 58.4% for discussion about alcohol use. The corresponding scores for the CMEP group were 95.8%, 97.6%, 77.6% and 64.6%. The changes in mean scores between phase 1 and phase 2 ranged from -1.9 to 2.3 points. There were no significant differences between the 2 groups in phase 1 or phase 2 scores or in change in scores. A total of 64.3% of the physicians rated the PAR as useful, 26.5% found the CMEP to be useful, and 41.0% considered the mentor strategy to be a useful form of continuing medical education. Although changes in practice related to the PAR, CMEP or mentor were reported by some physicians, they were not related to chart audit or patient scores. INTERPRETATION: Educational interventions based on quality-of-care assessments and directed to global improvements in quality of care did not result in improvements in the outcome measures. Educational interventions may have to be targeted to specific areas of the practice, with physicians being monitored and receiving ongoing feedback on their performance.
The effect of glycogen content on the activation of glycogen phosphorylase during adrenaline stimulation was investigated in soleus muscles from Wistar rats. Furthermore, adrenergic activation of glycogen phosphorylase in the slow-twitch oxidative soleus muscle was compared to the fast-twitch glycolytic epitrochlearis muscle. The glycogen content was 96.4 +/- 4.4 mmol (kg dw)(-1) in soleus muscles. Three hours of incubation with 10 mU/ml of insulin (and 5.5 mM glucose) increased the glycogen content to 182.2+/-5.9 mmol (kg dw)(-1) which is similar to that of epitrochlearis muscles (175.7+/-6.9 mmol (kg dw)(-1)). Total phosphorylase activity in soleus was independent of glycogen content. Adrenaline (10(-6) M) transformed about 20% and 35% (P < 0.01) of glycogen phosphorylase to the a form in soleus with normal and high glycogen content, respectively. In epitrochlearis, adrenaline stimulation transformed about 80% of glycogen phosphorylase to the a form. Glycogen synthase activation was reduced to low level in soleus muscles with both normal and high glycogen content. In conclusion, adrenaline-mediated glycogen phosphorylase activation is enhanced in rat soleus muscles with increased glycogen content. Glycogen phosphorylase activation during adrenaline stimulation was much higher in epitrochlearis than in soleus muscles with a similar content of glycogen.
The hypothalamic satiety peptide CART (cocaine and amphetamine regulated transcript) is expressed at high levels in anorectic rat glucagonomas but not in hypoglycemic insulinomas. However, a non-anorectic metastasis derived from the glucagonoma retained high CART expression levels and produced circulating CART levels comparable to that of the anorectic tumors. Moreover, distinct glucagonoma lines derived by stable HES-1 transfection of the insulinoma caused severe anorexia but retained low circulating levels of CART comparable to that of insulinoma bearing or control rats. Islet tumor associated anorexia and circulating CART levels are thus not correlated, and in line with this peripheral administration of CART (5-50 mg/kg) produced no effect on feeding behavior. In the rat two alternatively spliced forms of CART mRNA exist and quantitative PCR revealed expression of both forms in the hypothalamus, in the different islet tumors, and in the islets of Langerhans. Immunocytochemistry as well as in situ hybridization localized CART expression to the somatostatin producing islet D cell. A potential endocrine/paracrine role of islet CART remains to be clarified.
The somatostatin upstream enhancer (SMS-UE) is a highly complex enhancer element. The distal A-element contains overlapping Pdx1 and Pbx binding sites. However, a point mutation in the A-element that abolishes both Pdxl and Pbx binding does not impair promoter activity. In contrast, a point mutation that selectively eliminates Pdx1 binding to a proximal B-element reduces the promoter activity. The B-element completely overlaps with a Pax6 binding site, the C-element. A point mutation in the C-element demonstrates that Pax6 binding is essential for promoter activity. Interestingly, a block mutation in the A-element reduces both Pax6 binding and promoter activity. In heterologous cells, Pdx1 potentiated Pax6 mediated activation of a somatostatin reporter. We conclude that the beta/delta-cell-specific activity of the SMS-UE is achieved through simultaneous binding of Pdx1 and Pax6 to the B- and C-elements, respectively. Furthermore, the A-element appears to stabilise Pax6 binding.
Alpha-cell specific transcription of the glucagon gene is mainly conferred by the glucagon promoter G1-element, while additional elements G2, G3, and G4 have broad islet cell specificity. Transcription of the glucagon gene has been shown to be stimulated by Pax6 through binding to the glucagon gene promoter G3-element. In this report, we show that Pax6 additionally binds the glucagon gene promoter G1-element and forms a transcriptionally active complex with another homeodomain protein, Cdx2/3. Two distinct mutations in the G1-element, that both reduce promoter activity by 85-90%, is shown to eliminate binding of either Pax6 or Cdx2/3. Additionally, Pax6 enhanced Cdx2/3 mediated activation of a glucagon reporter in heterologous cells. We discuss how Pax6 may contribute to cell-type specific transcription in the pancreatic islets by complex formation with different transcription factors.
Linear alkylbenzene sulphonates (LAS) are a group of anionic surfactants, characterised by having both a hydrophobic and a hydrophilic group. LAS is one of the major ingredients of synthetic detergents and surfactants and is used world-wide for both domestic and industrial applications. LAS is relatively rapidly aerobically degraded, but only very slowly or not at all degraded under anaerobic conditions. Therefore, LAS can be found in very high concentrations in most sewage sludge and enter the soil compartment as a result of sludge application. LAS can be found in elevated concentrations in soil immediately after sludge amendment, but a half-life of approximately 1-3 weeks will generally prevent accumulation in soil and biota. The concentration in soils that have not received sewage sludge recently, is generally less than 1 mg kg-1 and not more than 5 mg LAS kg-1. This is below the lowest concentration of LAS where effects have been observed in the laboratory. The laboratory data is in accordance with field studies using aqueous solutions of the sodium salt of LAS. However, observations of the ecological impact of sewage sludge applications or application of LAS spiked into sludge indicates a lower toxicity of LAS when applied in sludge. On the basis of the information reviewed in this paper, it is concluded that LAS can be found in high concentrations in sewage sludge, but that the relatively rapid aerobic degradation and the reduced bioavailability when applied via sludge, most likely will prevent LAS from posing a threat to terrestrial ecosystems on a long term basis.
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OBJECTIVE: To compare infant feeding practices among low-income, urban, African-American women enrolled in the Special Supplemental Nutrition Program for Women, Infants, and Children (WIC) with current recommendations for infant feeding. DESIGN: Longitudinal follow-up of women and their infants who participated in a WIC-based breast-feeding promotion project. Women enrolled prenatally at or before 24 weeks of gestation were followed up until 16 weeks postpartum. SUBJECTS/SETTING: Two hundred seventeen African-American WIC participants in an urban area. METHODS: Data related to infant feeding practices were collected by interviewers who used a structured questionnaire to determine when nonmilk liquids or solids were introduced to the infant. Reported practices were compared with current recommendations. STATISTICAL ANALYSIS PERFORMED: Contingency table analysis, including chi 2 tests, and multivariate analysis using logistic regression. RESULTS: By 7 to 10 days postpartum, approximately a third of infants were receiving some nonmilk liquids or solids; this escalated to 77% by 8 weeks and 93% by 16 weeks postpartum. Women breast-feeding exclusively (i.e., not adding nonmilk liquids or solids) were least likely, and women providing mixed feeding (breast milk and formula) were more likely, than women feeding formula exclusively to introduce nonmilk liquids and solids at each data collection time period. APPLICATIONS/CONCLUSIONS: WIC participants who receive instruction about infant feeding nutrition are no more likely than mothers who do not participate in WIC to follow infant feeding guidelines recommended by the American Academy of Pediatrics in regard to the time when solids should be introduced to infants' diet. Our findings suggest the need for WIC to implement more powerful and innovative educational and motivational strategies to help mothers delay the introduction of nonmilk liquids and solid foods until their infants are 4 to 6 months old, as recommended.
The aim of this study was to investigate the internal and external validity of the Whiteley Index as a screening instrument for somatization illness. A 14-item version of the Whiteley Index for hypochondriacal traits was given to 99 of 191 consecutive primary care patients, aged 18-65 years, and to 100 consecutive patients, aged 18-60 years, admitted for the first time to a neurological ward. The primary care sample was, in addition, interviewed by means of the SCAN (Schedules for Clinical Assessment in Neuropsychiatry) psychiatric interview. The GPs and the neurologists were asked to rate various characteristics of the patients that might indicate somatization. The internal validity of the Whiteley Index was tested by means of latent structure analysis. On this basis, a reduced seven-item scale (Whiteley-7 scale) and two subscales (i.e., an Illness Conviction and Illness Worrying scale, each with three items) were constructed. All three had a high internal validity fitting into the very restricted Rasch statistical model (p>0.05) and an acceptable transferability between most of the subpopulations investigated. In the primary care population, the Whiteley-7 and the Illness Conviction scales at cut-point 0/1 showed 1.00 and 0.87 sensitivity and 0.65 and 0.87 specificity, respectively, using as "gold standard" the fulfillment of criteria for at least one ICD-10 somatoform disorder, and 0.71 and 0.63 sensitivity and 0.62 and 0.87 specificity, respectively, as gold standard for the fulfillment of criteria for at least one DSM-IV somatoform disorder, excluding the NOS diagnostic group. The Illness Worrying subscale showed less impressive performance in this respect. The agreement between the Whiteley-7 scale including the two subscales and neurologists' rating and the GPs' rating and the somatization subscale on the SCL-90 was modest or worse. It may be concluded that the Whiteley-7 scale and the Illness Conviction subscale had acceptable psychometric profiles, and both seem to be promising screening tools for not only hypochondriasis but also for somatoform disorders in general.
Erectile dysfunction and impotence has a high prevalence among male hypertensive patients. Whether this relates mainly to specific drug side effects or to primary pathogenic disorders is unknown. In the present study 101 male patients from our outpatient hypertension clinic answered detailed questionnaires about hypertension and sexual function. Patients with perceived impotence were offered a thorough penile evaluation and examination performed by specialists in the urology department. Twenty-seven (27%) men had impotence. The main cause of impotence was an arterial dysfunction (89%). The prevalence of impotence was related to the degree of secondary organ manifestation, reflected by World Health Organization (WHO) classification I-III (P = .01). Intermittent claudication (P = .001) and ischemic heart disease (P = .005) were the best determinants in this respect. Twelve impotent patients (44%) ascribed onset of impotence to drug initiation. A variety of drugs were incriminated in the occurrence of drug-induced impotence. In summary our results indicate that impotence in hypertensive men is caused mainly by penile arterial vascular changes, probably atherosclerosis. Drug-induced impotence could well be the result of blood pressure reduction itself and not specific drug side effects.
Several investigations have reported high frequencies of reading and writing disabilities in criminal populations. The aims of the present study were to assess the frequency of dyslexia among Swedish prison inmates and to relate dyslexia to other indices of neuropsychological functions. Sixty-three prison inmates with Swedish as their native language, age 19 to 57 years, were examined by interviews, tests of academic achievement, and neuropsychological assessment. Twenty-six (41%) were diagnosed as dyslexic. As expected, the dyslexic group performed more poorly on verbal tests as compared to the normal readers among the prison inmates, but they also performed more poorly on tests measuring nonverbal abilities. The dyslexic group had higher frequencies of paranoid and avoidant personality disorders compared to the nondyslexics. They also reported higher levels of anxiety and suspicion and a lower degree of socialization. Previous studies report low IQ to be associated with criminal propensity, supporting the interpretation that a double handicap (dyslexia and low IQ) increases the risk of entering a criminal career and remaining in it.
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Chemokines direct tissue invasion by specific leukocyte populations. Thus, chemokines may play a role in multiple sclerosis (MS), an idiopathic disorder in which the central nervous system (CNS) inflammatory reaction is largely restricted to mononuclear phagocytes and T cells. We asked whether specific chemokines were expressed in the CNS during acute demyelinating events by analyzing cerebrospinal fluid (CSF), whose composition reflects the CNS extracellular space. During MS attacks, we found elevated CSF levels of three chemokines that act toward T cells and mononuclear phagocytes: interferon-gamma-inducible protein of 10 kDa (IP-10); monokine induced by interferon-gamma (Mig); and regulated on activation, normal T-cell expressed and secreted (RANTES). We then investigated whether specific chemokine receptors were expressed by infiltrating cells in demyelinating MS brain lesions and in CSF. CXCR3, an IP-10/Mig receptor, was expressed on lymphocytic cells in virtually every perivascular inflammatory infiltrate in active MS lesions. CCR5, a RANTES receptor, was detected on lymphocytic cells, macrophages, and microglia in actively demyelinating MS brain lesions. Compared with circulating T cells, CSF T cells were significantly enriched for cells expressing CXCR3 or CCR5. Our results imply pathogenic roles for specific chemokine-chemokine receptor interactions in MS and suggest new molecular targets for therapeutic intervention.
To examine how individuals within a woman's life influence her infant feeding intention, we interviewed 441 African-American women on the breastfeeding attitudes and experiences of their friends, relatives, mother, and the baby's father. Women were interviewed at entry into prenatal care at clinics associated with one of four Baltimore WIC clinics chosen for a breastfeeding promotion project. Qualitative data were also collected among 80 women. Friends and "other" relatives were not influential. Grandmothers' opinions and experiences were important, but their influence was reduced after considering the opinion of the baby's father. The opinion of the woman's doctor was an independent predictor of infant feeding intention. Breastfeeding promotion programs should recognize the separate influence of fathers, health providers, and grandmothers in women's infant feeding decisions.
When including clinical mastitis in the breeding goal, it is useful to know what measure of the trait is most appropriate and its relationship to the primary production traits and indicator traits in the relevant population. In this paper, genetic and phenotypic parameters for clinical mastitis, somatic cell production deviance, and protein yield were estimated for the dairy breed Danish Red. In preliminary analyses, the heritability for clinical mastitis was found to be highest in early lactation, and its genetic correlation to clinical mastitis at other stages of lactation were high. Therefore, clinical mastitis defined in early lactation was the measure of clinical mastitis used in subsequent analyses. Two bivariate analyses were performed. Each analysis fitted clinical mastitis and either somatic cell production deviance or protein yield as a continuous trait. The bivariate model was composed of a Gaussian model for the continuous trait and a threshold model for mastitis. The analyses were performed in a Bayesian setting, using the Gibbs sampler. Point estimates (mean of marginal posterior densities) of heritability for mastitis on the underlying scale were estimated to be 0.10 and 0.12 in the two analyses. The genetic correlation between mastitis and protein yield was 0.43 and between mastitis and somatic cell production deviance was 0.80. These results make clear the importance of including clinical mastitis in the breeding goal and the usefulness of somatic cell production deviance as the indicator trait for clinical mastitis. The best measure of clinical mastitis was to consider only cases in early lactation.
Only a few studies have been published on the postprandial effects of different fatty acids in obese subjects. Therefore, the present study investigated the effects of three test meals containing palm oil (PO), lard (LD), or puff-pastry margarine (PPM), all normal dietary ingredients, on postprandial lipid and hormone responses in normal-weight and obese young women. The study was performed as a randomized, crossover design. The fats differed in the content of palmitic acid, stearic acid, and trans monounsaturated fatty acids allowing a dietary comparison of different 'solid' fatty acids. The obese women had significantly higher fasting concentrations and postprandial responses of plasma total triacylglycerol (TAG), chylomicron-TAG, and insulin compared with the normal-weight women but there was no significant difference in the postprandial responses between the three test meals. The obese women had fasting concentrations of leptin four times greater than the normal-weight women. There were no postprandial changes in the concentrations of leptin. The fasting concentrations of HDL-cholesterol were significantly lower in the obese women than in the normal-weight women, whereas there was no significant difference between the two groups in the concentrations of total cholesterol or LDL-cholesterol. These results provide evidence that obese women have exaggerated lipid and hormone responses compared with normal-weight women but the different contents of saturated and trans monounsaturated fatty acids provided by PO, LD, and PPM have no effect in either group.