Occult cardiac tamponade detected by transesophageal echocardiography.

Transesophageal echocardiography is a safe, minimally invasive procedure that should be considered when the diagnosis of cardiac tamponade is a possibility and when conventional methods fail to provide conclusive diagnostic information. In this report, we describe a 74-year-old man in the intensive-care unit whose condition was unstable postoperatively because of an occult loculated pericardial effusion and cardiac tamponade. Routine noninvasive and invasive monitoring, including hemodynamic monitoring and transthoracic echocardiography, failed to confirm definitively the suspected diagnosis of cardiac tamponade. In addition, because of the hemodynamic instability of the patient, transporting him for definitive tests (such as fast computed tomographic scanning of the mediastinum, which could not be performed at the bedside) for assessment of cardiac tamponade was relatively contraindicated. In our patient, the diagnostic information obtained by transesophageal echocardiography may have been lifesaving.     

Boundary Ambiguity in Parents With Chronically Ill Children: Integrating Theory and Research

Abstract: This article integrates theory and research related to boundary ambiguity in parents of children with a chronic health condition. We propose that boundary ambiguity is a risk factor for psychological distress in these parents. Clinical applications and a case example highlight how boundary ambiguity can be assessed and managed in clinical settings by professionals working with parents with chronically ill children. Questions are provided for assessing boundary ambiguity in clinical and research settings, and implications for research are discussed.     

Serum albumin and self-reported prevalence of stroke: a population-based, cross-sectional study.

BACKGROUND: Since information about the association between serum albumin and risk of stroke is limited the purpose of the present paper was to re-investigate this relationship. DESIGN: The study followed a cross-sectional design. METHODS: In the cross-sectional Norwegian Oslo Health Study the concentration of serum albumin and blood pressure was determined in a random sample of 5071 men and women, 30-75 years of age. Logistic regression was used to study the association between the serum albumin concentration and self-reported prevalence of stroke. In the sample there were 122 subjects with a history of stroke and 4949 subjects without. RESULTS: Low albumin (i.e. < or =47 versus >47 g/l) was associated with increased prevalence of self-reported stroke (odds ratio 1.83; 95% confidence interval, 1.20-2.78; P=0.005), after adjusting for age (< or =45 versus > or =59 years) and sex. Including smoking, blood pressure and length of education into the model did not have any major influence on the result. CONCLUSION: Low serum albumin is associated with increased prevalence of self-reported stroke.     

Scale-up of Adhesive Transdermal Drug Delivery Systems

Pharmaceutical Research -     

Mechanisms by which the putative serotonin receptor antagonist metitepin alters nociception in mice

Summary The putative serotonin (5-HT) receptor antagonist metitepin (0.5 mg/ kg, intraperitoneally) produced hypoalgesia in the increasing temperature hot-plate test and hyperalgesia in the tail-flick test in mice. The effects of metitepin were not altered after depletion of 5-HT by the neurotoxin 5,7-dihydroxytryptamine (5, 7-DHT, 80 g free base, intracerebroventricularly) or the serotonin synthesis inhibitor p-chlorophenylalanine (PCPA, 400 mg/kg for 10 consecutive days). After chronic administration (2 or 5 mg/kg for 18 consecutive days) tolerance to the effect of metitepin (0.5 mg/kg) and cross-tolerance to the antinociceptive effect of the 5-HT agonist 5-methoxy-N,N-dimethyltryptamine (5-MeODMT, 3 mg/kg) was found in the hot-plate test but not in the tail-flick test. It is suggested that metitepin may block descending 5-HT transmission while more complex mechanisms of action are involved at supraspinal level. One possibility is that metitepin exhibits partial agonist properties or, alternatively, that the drug may block 5-HT subsystems which tonically enhance nociception.     

Laforin preferentially binds the neurotoxic starch-like polyglucosans, which form in its absence in progressive myoclonus epilepsy

Lafora disease (LD) is a fatal and the most common form of adolescent-onset progressive epilepsy. Fulminant endoplasmic reticulum (ER)-associated depositions of starch-like long-stranded, poorly branched glycogen molecules [known as polyglucosans, which accumulate to form Lafora bodies (LBs)] are seen in neuronal perikarya and dendrites, liver, skeletal muscle and heart. The disease is caused by loss of function of the laforin dual-specificity phosphatase or the malin E3 ubiquitin ligase. Towards understanding the pathogenesis of polyglucosans in LD, we generated a transgenic mouse overexpressing inactivated laforin to trap normal laforin's unknown substrate. The trap was successful and LBs formed in liver, muscle, neuronal perikarya and dendrites. Using immunogold electron microscopy, we show that laforin is found in close proximity to the ER surrounding the polyglucosan accumulations. In neurons, it compartmentalizes to perikaryon and dendrites and not to axons. Importantly, it binds polyglucosans, establishing for the first time a direct association between the disease-defining storage product and disease protein. It preferentially binds polyglucosans over glycogen in vivo and starch over glycogen in vitro, suggesting that laforin's role begins after the appearance of polyglucosans and that the laforin pathway is involved in monitoring for and then preventing the formation of polyglucosans. In addition, we show that the laforin interacting protein, EPM2AIP1, also localizes on the polyglucosan masses, and we confirm laforin's intense binding to LBs in human LD biopsy material.     

Cardiovascular risk factors in people with different genotypes in the insertion/deletion (I/D) polymorphism at the locus for angiotensin I-converting enzyme (ACE)

The deletion (D) allele of an insertion/deletion (I/D) polymorphism at the locus for angiotensin I-converting enzyme (ACE) has been reported to be an independent risk factor for myocardial infarction (MI), particularly in people lacking traditional risk factors. Furthermore, a borderline association between Lp(a) lipoprotein level and the I/D polymorphism at the ACE locus was reported in one study. We have searched for possible "level gene" or "variability gene" effects of ACE genes on Lp(a) lipoprotein, total cholesterol (TC), high density lipoprotein (HDL) cholesterol (HDLC), low density lipoprotein (LDL) cholesterol (LDLC), triglycerides (TG), apolipoprotein B (apoB), apolipoprotein A-I (apoA-I), and body mass index (BMI). None of these variables differed significantly between genotypes in the I/D polymorphism in any of three population samples. A single population sample created by combining the three series, exhibited an insignificant trend towards individuals carrying the D-allele having a higher level of Lp(a) lipoprotein than those lacking it, and DD homozygotes had a significantly higher Lp(a) lipoprotein level than the combined group of ID/II individuals (p = 0.03). These results may indicate that the D-allele of the I/D polymorphism at the ACE locus could influence the level of Lp(a) lipoprotein.     

Synergistic effect of a combination of nicarbazin and monensin against coccidiosis in the chicken caused by Eimeria spp.

ABSTRACT

A clinical study was made into the abilities of nicarbazin and monensin and a nicarbazin?+?monensin combination to control Eimeria acervulina, E. maxima, and E. tenella in chickens. When included in the feed, at concentrations of 40?ppm nicarbazin or 40?ppm monensin, these products showed partial efficacy evaluated by daily weight gain (DWG) but no activity judged by daily feed intake (DFI) or feed conversion ratio (FCR). By contrast, the combination of 40?ppm nicarbazin?+?40?ppm monensin provided complete control of infection judged by greater DWG and DFI, and lower FCR. Monensin at a concentration of 40?ppm was ineffective in preventing lesions caused by all three species. Nicarbazin at a concentration of 40?ppm was unable to suppress lesions of E. acervulina and E. maxima but was able to suppress lesions caused by E. tenella. Nicarbazin 40?ppm?+?monensin 40?ppm suppressed lesions of all three species.

RESEARCH HIGHLIGHTS

• Nicarbazin or monensin at 40 ppm gave only partial control of Eimeria spp.

• A combination of 40 ppm nicarbazin + 40 ppm monensin controlled DWG, DFI and FCR.

• Nicarbazin or monensin at 40 ppm did not suppress all Eimeria spp. lesions.

• Nicarbazin 40 ppm + monensin 40 ppm suppressed lesions of all three species.

     

The CD8+ granzyme B+ T-cell subset in peripheral blood from healthy individuals contains activated and apoptosis-prone cells.

Granzyme B (GrB) has been implicated in induction of apoptosis in target cells. The presence of GrB in peripheral blood CD8+ T cells from healthy individuals was analysed in immunocytochemical and flow cytometric studies. Furthermore, CD8+ GrB- T cells and CD8+ GrB+ T cells were compared regarding phenotypical characteristics and susceptibility to both spontaneous and Fasmediated apoptosis. GrB was expressed by approximately one-fifth of CD8+ T cells. Compared with the CD8+ GrB- T-cell subset, the CD8+ GrB+ T-cell subset contained cells that were relatively more activated and more prone to spontaneous apoptosis. Culturing of cells with immunoglobulin M (IgM) anti-Fas monoclonal antibody had no additional effect on the number of CD8+ GrB+ T cells undergoing apoptosis. We suggest that the presence of CD8+ GrB+ T cells in peripheral blood from healthy individuals results from immune surveillance or contact with infectious agents, and that spontaneous apoptosis of these cells might serve as a mechanism for their eventual clearance.