Miracle-dz/UniFAR-FTUs huggingface dataset:
Day surgery for breast cancer: effects of a psychoeducational telephone intervention on functional status and emotional distress.

PURPOSE/OBJECTIVES To determine the efficacy of a nursing intervention based on self-regulation theory known as the Attentional Focus and Symptom Management Intervention (AFSMI) in enhancing physical and emotional well-being in women who underwent day surgery for breast cancer. DESIGN Randomized clinical block trial; subjects were randomly allocated to the experimental group (n = 61) or the usual care (control) group (n = 56). Subjects in the experimental group received the AFSMI during two phone sessions, at 3-4 days and 10-11 days after surgery. SETTING The convenience sample was drawn from five regional centers located in different geographic areas (urban and rural regions) in Quebec, Canada. SAMPLE 117 patients with primary breast cancer who underwent day surgery as part of their initial treatment for cancer. METHODS Data collection and nursing intervention via telephone interviews. MAIN RESEARCH VARIABLES Functional status and emotional distress. FINDINGS Significant differences between the experimental and control group were found at post-test on home management, total mood disturbance, confusion, and tension scores. CONCLUSIONS The AFSMI was effective in reducing emotional distress and enhancing physical functioning. IMPLICATIONS FOR NURSING Findings validate the use of the self-regulation model in designing individualized nursing interventions. Redirecting attention and focusing on concrete objective features hold potential in developing other innovative nursing interventions.
Role of Complement in the Induction of Immunological Responses

The importance of complement as a mediator of the effects of allergic reactions and of non-immunological inflammation is well recognised. In contrast to this efferent or effector role, the idea that complement might also play a part in induction of the allergic response, that is the afferent limb of immunological function, was suggested by two sets of observations. First the demonstration by Nussenzweig and his colleagues of receptors for fixed C3 on the surface of B lymphocytes, (Bianco, Patrick & Nussenzweig 1970), and second, the detection by Gajl-Peczalska et al. (1969) of C3 and complement-fixing immune complexes within germinal centers of lymphoid follicles. The first experimental evidence for such a role of complement was the in vivo suppressive effect on thymus-dependent antibody production in mice (Pepys 1972a) of the complement-activating protein (cobra factor, CoF) of cobra (Naja naja) venom (Nelson 1966, Ballow & Cochrane 1969). This led to the hypothesis that complement might participate in cooperative antibody production (Pepys 1972a, 1973, 1974a) and there has since been further exploration of this concept at the experimental and at the theoretical level. The aim of this review is to evaluate the various observations and assertions made to date.
Determination of enoxaparin with rotational thrombelastometry using the prothrombinase-induced clotting time reagent

Drug monitoring of low molecular weight heparin is generally not recommended, but could be reasonable in critically ill patients, whose risk for bleeding or thrombosis shows a high interpatient variability. Anti-Xa assays are not available around the clock even in central hospitals, whereas rotational thrombelastometry (ROTEM) becomes increasingly used at the bedside. Prothrombinase-induced clotting time (PiCT) reagent allows determination of factor Xa-inhibition in plasma. The aim of our study was to evaluate enoxaparin determination in whole blood with the ROTEM using specific test modifications, including PiCT. After ethics committee's approval, citrated whole blood obtained from overall 16 healthy volunteers was incubated with enoxaparin at 16 different anti-Xa concentrations. Main endpoint was the clotting time (CT) in ROTEM representing initial activation of clot formation. CT was determined in the new PiCT-ROTEM test, in a low-tissue factor-activated modification (LowTF-ROTEM) as well as in the commercially available heparin-sensitive ROTEM assays (HEPTEM and INTEM). In the absence of enoxaparin, CT values were 168.6 ± 6.1 s (PiCT-ROTEM), 247.3 ± 18.6 s (LowTF-ROTEM), and –6.2 ± 7.9 s (INTEM-HEPTEM). A linear dependency (P < 0.01) between anti-Xa concentration and CT was found for PiCT-ROTEM, LowTF-ROTEM, and for INTEM-HEPTEM with correlation coefficients of 0.93 for PiCT-ROTEM, 0.94 for LowTF-ROTEM, and 0.81 for INTEM-HEPTEM. This in-vitro experiment demonstrates a strong correlation between enoxaparin anti-Xa concentrations and specific ROTEM tests. These promising assays should be further evaluated for monitoring anticoagulation in high-risk patients in clinical studies.
Drug–drug interactions between anti-retroviral therapies and drugs of abuse in HIV systems

Introduction: Substance abuse is a common problem among HIV-infected individuals. Importantly, addictions as well as moderate use of alcohol, smoking, or other illicit drugs have been identified as major reasons for non-adherence to antiretroviral therapy (ART) among HIV patients. The literature also suggests a decrease in the response to ART among HIV patients who use these substances, leading to failure to achieve optimal virological response and increased disease progression. Areas covered: This review discusses the challenges with adherence to ART as well as observed drug interactions and known toxicities with major drugs of abuse, such as alcohol, smoking, methamphetamine, cocaine, marijuana, and opioids. The lack of adherence and drug interactions potentially lead to decreased efficacy of ART drugs and increased ART, and drugs of abuse-mediated toxicity. As CYP is the common pathway in metabolizing both ART and drugs of abuse, we discuss the possible involvement of CYP pathways in such drug interactions. Expert opinion: We acknowledge that further studies focusing on common metabolic pathways involving CYP and advance research in this area would help to potentially develop novel/alternate interventions and drug dose/regimen adjustments to improve medication outcomes in HIV patients who consume drugs of abuse.
Pityriasis Rubra Pilaris in Childhood: A Long‐term Study of 29 Cases

Abstract: Pityriasis rubra pilaris (PRP) is a dermatosis of unknown origin with a limited frequency in childhood (0.2% of our hospitalized pediatric patients). During the last 20 years we have observed 31 new cases; follow‐up has been conducted in 29 children. The acute self‐resolving form seems to be the most frequent in children, compared to adults. No cases of hereditary PRP have been observed, and no relationship between the severity of PRP and its prognosis has been reported. Since juvenile PRP has a relatively rapid course and a spontaneous resolution (a few months), it seems unnecessary to use potentially harmful drugs. Synthetic retinoids may be employed in patients whose disease is both persistent and disabling.
Ever shorter telomere 1 (EST1)-dependent reverse transcription by Candida telomerase in vitro: Evidence in support of an activating function

Telomerase is an RNA–protein complex responsible for the extension of one strand of the telomere terminal repeats. Analysis of the telomerase complex in the budding yeast Saccharomyces cerevisiae has revealed the presence of one catalytic protein subunit (Est2p/TERT) and at least two noncatalytic components (Est1p and Est3p). The TERT subunit is essential for telomerase function, both in vitro and in vivo. In contrast, the Est1p and Est3p subunits, although required for telomere extension in vivo, have not been shown to affect enzyme activity in vitro. We recently identified orthologues of the Saccharomyces telomerase subunits in Candida albicans (named CaTERT, CaEst1p, and CaEst3p). Analysis of telomerase from the Candida Caest1-Δ strains revealed a primer-specific defect in its activity in vitro: The mutant enzyme was impaired in its ability to extend some, but not all, telomeric primers. The CaEst1p-responsive primers have 3′ ends that are clustered in two loci within the 23-bp Candida telomere repeat. The degree of CaEst1p-dependence was modulated by the length and sequence of the 5′ ends. For CaEst1p-dependent primers, the wild-type enzyme consistently exhibited a greater Vmax than the mutant enzyme in kinetic studies. These results suggest that CaEst1p augments the ability of telomerase to reverse-transcribe through selected barriers in the telomere repeat by acting as an allosteric activator and provide the basis for a functional in vitro assay for a noncatalytic protein component of the telomerase complex.
The histone‐like protein HU binds specifically to DNA recombination and repair intermediates

The heterodimeric HU protein associated with the Escherichia coli nucleoid shares some properties with histones and HMG proteins. HU binds DNA junctions and DNA containing a nick much more avidly than double‐stranded (ds‐) DNA. Cells lacking HU are extremely sensitive to γ irradiation and we wondered how HU could play a role in maintaining the integrity of the bacterial chromosome. We show that HU binds with high affinity to DNA repair and recombination intermediates, including DNA invasions, DNA overhangs and DNA forks. The DNA structural motif that HU specifically recognizes in all these structures consists of a ds‐DNA module joined to a second module containing either ds‐ or single‐stranded (ss‐) DNA. The two modules rotate freely relative to one another. Binding specificity results from the simultaneous interaction of HU with these two modules: HU arms bind the ds‐DNA module whereas the HU body contacts the 'variable' module containing either ds‐ or ss‐DNA. Both structural motifs are recognized by HU at least 1000‐fold more avidly than duplex DNA.
Comparison of thrombophilic gene mutations among patients experiencing recurrent miscarriage and deep vein thrombosis.

PROBLEM Inherited thrombophilia has been shown to be a risk factor for cardiovascular disease including deep venous thrombosis as well as reproductive disorders including recurrent pregnancy loss. We have previously reported three out of the 10 thrombophilic mutations studied, plasminogen activator inhibitor-1 (PAI-1) 4G/5G, factor XIII V34L, and homozygous MTHFR C667T, correlated significantly with recurrent pregnancy loss compared with controls. This study was undertaken to compare the frequencies of nine inherited thrombophilias among women with a history of recurrent pregnancy loss with individuals experiencing deep venous thrombosis and fertile controls. METHOD OF STUDY Six hundred thirty-four participants including 550 women with a history of recurrent pregnancy loss, 43 individuals with deep vein thrombosis and 41 fertile women without a history of recurrent miscarriage. All participants had buccal swabs taken for DNA analyses of nine gene polymorphisms including factor V G1691A, factor V H1299R (R2), factor II Prothrombin G20210A, factor XIII V34L, beta-fibrinogen -455G>A, PAI-1 4G/5G, human platelet antigen 1 a/b (L33P), MTHFR C677T, MTHFR A1298C. Frequencies of thrombophilic gene polymorphisms were compared among the three populations studied. RESULTS Individuals with a history of DVT had a significantly higher frequency of all of the polymorphisms studied compared with women experiencing a history of recurrent pregnancy loss and the fertile controls. The frequencies of mutations for V34L and PAI-1 4G/5G were significantly increased among women experiencing recurrent pregnancy loss compared with controls. The most prevalent polymorphisms were factor XIII V34L and PAI-1 4G/4G for both individuals with a history of deep vein thrombosis and recurrent pregnancy loss compared with controls. CONCLUSION Screening for risk factors for inherited thrombophilia with only polymorphisms for factor V von Leiden, factor II prothrombin and MTHFR may be missing the more prevalent identifiers of jeopardy.
Neurogenic inflammation in the context of migraine

Despite considerable research into the pathogenesis of idiopathic headaches, such as migraine, the pathophysiological mechanisms underlying them remain poorly understood. Although it is well established that the trigeminal nerve becomes activated during migraine, the consequences of this activation remain controversial. One theory, based on preclinical observations, is that activation of trigeminal sensory fibers leads to a painful neurogenic inflammation within the meningeal (dural) vasculature mediated by neuropeptide release from trigeminal sensory fibres and characterized by plasma protein extravasation, vasodilation, and mast cell degranulation. Effective antimigraine agents such as ergots, triptans, opioids, and valproate inhibit preclinical neurogenic dural extravasation, suggesting that this activity may be a predictor of potential clinical efficacy of novel agents. However, several clinical trials with other agents that inhibit this process preclinically have failed to show efficacy in the acute treatment of migraine in man. Alternatively, it has been proposed that painful neurogenic vasodilation of meningeal blood vessels could be a key component of the inflammatory process during migraine headache. This view is supported by the observation that jugular plasma levels of the potent vasodilator, calcitonin gene‐related peptide (CGRP) are elevated during the headache and normalized by successful sumatriptan treatment. Preclinically, activation of trigeminal sensory fibers evokes a CGRP‐mediated neurogenic dural vasodilation, which is blocked by dihydroergotamine, triptans, and opioids but unaffected by NK1 receptor antagonists that failed in clinical trials. These observations suggest that CGRP release with associated neurogenic dural vasodilation may be important in the generation of migraine pain, a theory that would ultimately be tested by the clinical testing of a CGRP receptor antagonist. Microsc. Res. Tech. 53:167–178, 2001. © 2001 Wiley‐Liss, Inc.
Tat‐Hsp70 protects dopaminergic neurons in midbrain cultures and in the substantia nigra in models of Parkinson’s disease

Parkinson’s disease is characterized by the progressive loss of dopaminergic (DA) neurons in the substantia nigra. The heat‐shock protein 70 (Hsp70) reduces protein misfolding and aggregation. It has been shown to protect cells against oxidative stress and apoptotic stimuli in various neurodegenerative disease models. To deliver Hsp70 across cellular membranes and into the brain, we linked it to a cell‐penetrating peptide derived from the HIV trans‐activator of transcription (Tat) protein. In vitro, Tat‐Hsp70 transduced neuroblastoma cells and protected primary mesencephalic DA neurons and their neurites against MPP+‐mediated degeneration. In vivo, the systemic application of cell‐permeable Hsp70 protected DA neurons of the substantia nigra pars compacta against subacute toxicity of MPTP. Furthermore, Tat‐Hsp70 diminished the MPTP induced decrease in DA striatal fiber density. Thus, we demonstrate that systemically applied Tat‐Hsp70 effectively prevents neuronal cell death in in vitro and in vivo models of Parkinson’s disease. The use of Tat‐fusion proteins might therefore be a valuable tool to deliver molecular chaperones like Hsp70 into the brain and may be the starting point for new protective strategies in neurodegenerative diseases.
Predictors of Research Use Among Staff in Aboriginal Addiction Treatment Programs Serving Women

The objective of this study was to identify the predictors of research use among staff from Aboriginal addiction programs serving women. A total of 89 staff from 26 Aboriginal addiction programs completed an online survey that included items assessing the theory of planned behavior constructs (attitudes, subjective norms, perceived behavioral control), intent to use research, and research use. Consistent with the theory of planned behavior, research use was predicted by attitudes, subjective norms, and perceived behavioral control. Intent to use research was not a mediator, demonstrating partial applicability of the theory of planned behavior to staff in Aboriginal addiction programs serving women.
A new method for back lobe suppression of microstrip leaky-wave antenna

In this paper, a new method for back lobe suppression of microstrip leaky-wave antenna (MLWA) is proposed. By adding microstrip dipole antennas above the MLWA, the radiation efficiency of MLWA is improved, and the reflected back lobe of MLWA is suppressed. The finite difference time domain (FDTD) method is used to simulate this MLWA. With a length of 2 wave-length of MLWA the back lobe is suppressed to -10.6 dB at 10.5 GHz, which is 8.6 dB lower than conventional MLWA.
Expression of Immunoglobulin Receptors with Distinctive Features Indicating Antigen Selection by Marginal Zone B Cells from Human Spleen

Marginal zone (MZ) B cells, identified as surface (s)IgMhighsIgDlowCD23low/−CD21+CD38− B cells, were purified from human spleens, and the features of their V(D)J gene rearrangements were investigated and compared with those of germinal center (GC), follicular mantle (FM) and switched memory (SM) B cells. Most MZ B cells were CD27+ and exhibited somatic hypermutations (SHM), although to a lower extent than SM B cells. Moreover, among MZ B-cell rearrangements, recurrent sequences were observed, some of which displayed intraclonal diversification. The same diversifying sequences were detected in very low numbers in GC and FM B cells and only when a highly sensitive, gene-specific polymerase chain reaction was used. This result indicates that MZ B cells could expand and diversify in situ and also suggested the presence of a number of activation-induced cytidine deaminase (AID)-expressing B cells in the MZ. The notion of antigen-driven expansion/selection in situ is further supported by the VH CDR3 features of MZ B cells with highly conserved amino acids at specific positions and by the finding of shared (“stereotyped”) sequences in two different spleens. Collectively, the data are consistent with the notion that MZ B cells are a special subset selected by in situ antigenic stimuli.
Design and Dynamic Culture of 3D-Scaffolds for Cartilage Tissue Engineering

Engineered scaffolds for tissue-engineering should be designed to match the stiffness and strength of healthy tissues while maintaining an interconnected pore network and a reasonable porosity. In this work, we have used 3D-plotting technique to produce poly-L-Lactide macroporous scaffolds with two different pore sizes. The ability of these macroporous scaffolds to support chondrocyte attachment and viability were compared under static and dynamic loading in vitro. Moreover, the 3D-plotting technique was combined with porogen-leaching, leading to macro/microporous scaffolds, so as to examine the effect of microporosity on the level of cell attachment and viability under similar loading condition. Canine chondrocytes’ cells were seeded onto the scaffolds with different topologies, and the constructs were cultured for up to 2 weeks under static conditions or in a bioreactor under dynamic compressive strain of 10% strain, at a frequency of 1 Hz. The attachment and cell growth of chondrocytes were examined by scanning electron microscopy and by 3-(4,5-dimethythiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. A significant difference in cell attachment was observed in macroporous scaffolds with different pore sizes after 1, 7, and 14 days. Cell viability in the scaffolds was enhanced with decreasing pore size and increasing microporosity level throughout the culture period. Chondrocyte viability in the scaffolds cultured under dynamic loading was significantly higher (p<0.05) than the scaffolds cultured statically. Dynamic cell culture of the scaffolds improved cell viability and decreased the time of in vitro culture when compared to statically cultured constructs. Optimizing the culture conditions and scaffold properties could generate optimal tissue/constructs combination for cartilage repair.
Observations on Burnout in Family Medicine and Psychiatry Residents

ObjectiveTo investigate the relationship between burnout, work environment, and a variety of personalvariables, including age, gender, marital, parental and acculturation status within a population of family medicine and psychiatry resident physicians.MethodsBetween 2002 and 2005, 155 residents in family medicine and psychiatry at East Tennessee State University College of Medicine were surveyed at intervals using the Maslach Burnout Inventory and Work Environment Scale, form R, to assess their current state of emotional health and job satisfaction.ResultsFemale residents had lower scores on the Depersonalization scale of the Maslach Burnout Inventory (t = 3.37, p = 0.001). Parenting was associated with lower Depersonalization (t = 3.98, p<0.001) and Emotional Exhaustion (t = 2.59, p = 0.011). Residents from the United States culture reported higher Depersonalization and Emotional Exhaustion (t = −3.64, p<0.001; t = −3.85, p<0.001). On the Work Environment Scale, residents from United States culture reported less Task Orientation and Control but higher Work Pressure (t = 2.89, p = 0.005; t = 2.24, p = 0.027; t = −2.79, p = 0.006). Psychiatry residents reported less burnout than family medicine residents on the Depersonalization and Emotional Exhaustion scales (t = 2.49, p = 0.014: t = 2.05, p = 0.042) and higher Physical Comfort on the Work Environment Scale (t = −2.60,p = 0.011); while family medicine residents reported higher Peer Cohesion, Supervisor Support, and Autonomy (t = 3.41, p = 0.001; t = 2.38, p= 0.019; t = 2.27, p = 0.025). ConclusionThis study design, using well established, standard, and valid measures, identified important issues for further exploration: the relationship between acculturation to burnout the potential role of parenting as a protective factor from burnout, and the recognition that women residents may not be as vulnerable to burnout as previously reported.
Cholinergic denervation occurs early in Parkinson disease

Although Parkinson disease (PD) is viewed traditionally as a motor syndrome secondary to nigrostriatal dopaminergic denervation, recent studies emphasize nonmotor features. Nonmotor comorbidity, such as cognitive impairment, can be explained better by multisystem neurodegeneration that extends beyond the loss of dopaminergic nigral neurons.1 Lewy2 first identified the eponymous Lewy body in neurons of the nucleus basalis of Meynert, the source of cholinergic innervation of the cerebral cortex. There is considerable evidence for altered cholinergic neurotransmission in PD. In the Braak et al.3 staging scheme of PD pathology, nigral and basal forebrain pathology occur simultaneously. Loss of cholinergic forebrain neurons in PD postmortem specimens is of similar magnitude or greater than loss found in Alzheimer disease (AD). 4 A postmortem study found greater reductions of acetylcholinesterase (AChE) in the frontal cortex of patients with dementia compared to patients without dementia with PD.5 The development of PET technology to measure AChE functional activity offers the opportunity to study cholinergic innervation in vivo at early stages of neurodegenerative disorders. In this issue of Neurology ®, …