Miracle-dz/UniFAR-FTUs huggingface dataset:
Therapeutic Change in Group Therapy For Interpersonal Trauma: A Relational Framework for Research and Clinical Practice

Our understanding of therapeutic change processes in group therapy for complex interpersonal trauma has been limited. The present study aimed at addressing this gap by developing a framework of therapeutic change in this field from a survivor and therapist perspective. This is a qualitative study, which utilized semistructured individual interviews. Transcripts were analyzed using interpretative phenomenological analysis (IPA) to identify recurrent themes. A final sample of n = 16 patients and n = 5 facilitators completed the interview. Main change processes identified by survivors were as follows: self versus others, trust versus threat, confrontation versus avoidance, and “patching up” versus true healing. Therapeutic processes identified by therapist facilitators included managing group dynamics, unpredictability and uncertainty, and process versus content. The proposed framework explains therapeutic change in group therapy in relational terms, that is, therapeutic dissonance, the dynamic interaction of self and experience as well as building empathic trusting relations. The importance of managing dissonance to aid personally meaningful recovery was highlighted. These findings have implications for the usefulness of relational and person-centered approaches to clinical practice in the area of interpersonal and complex trauma, especially in the early identification, prevention, and management of dropouts.
CHC22 and CHC17 clathrins have distinct biochemical properties and display differential regulation and function

Clathrins are cytoplasmic proteins that play essential roles in endocytosis and other membrane traffic pathways. Upon recruitment to intracellular membranes, the canonical clathrin triskelion assembles into a polyhedral protein coat that facilitates vesicle formation and captures cargo molecules for transport. The triskelion is formed by trimerization of three clathrin heavy-chain subunits. Most vertebrates have two isoforms of clathrin heavy chains, CHC17 and CHC22, generating two clathrins with distinct cellular functions. CHC17 forms vesicles at the plasma membrane for receptor-mediated endocytosis and at the trans-Golgi network for organelle biogenesis. CHC22 plays a key role in intracellular targeting of the insulin-regulated glucose transporter 4 (GLUT4), accumulates at the site of GLUT4 sequestration during insulin resistance, and has also been implicated in neuronal development. Here, we demonstrate that CHC22 and CHC17 share morphological features, in that CHC22 forms a triskelion and latticed vesicle coats. However, cellular CHC22-coated vesicles were distinct from those formed by CHC17. The CHC22 coat was more stable to pH change and was not removed by the enzyme complex that disassembles the CHC17 coat. Moreover, the two clathrins were differentially recruited to membranes by adaptors, and CHC22 did not support vesicle formation or transferrin endocytosis at the plasma membrane in the presence or absence of CHC17. Our findings provide biochemical evidence for separate regulation and distinct functional niches for CHC17 and CHC22 in human cells. Furthermore, the greater stability of the CHC22 coat relative to the CHC17 coat may be relevant to its excessive accumulation with GLUT4 during insulin resistance.
Rapid weight loss alters muscular performance and perceived exertion as well as postural control in elite wrestlers.

AIM The aim was to assess the effects of rapid decline of body mass on postural control, muscular performance and rating perceived exertion in elite free style wrestlers. METHODS Ten high-level wrestlers (age: 19.3 ± 2.5 years, height: 175.7 ± 4.9 cm, body mass before dieting: 77.16 ± 11.94 kg) are included in the present study. Diet was monitored for all the athletes. Athropometric measurements and a variety of functional tests such as isometric hand grip strength (IHG) and isometric back strength (IBS) with dynamometers, dynamic postural control (DPC) with star excursion balance test, and rating of perceived exertion (RPE) to a standard exercise of knee pushups, were performed before and after diet completion. RESULTS The diet was based on food restriction and dehydration. Body mass, lean body mass and body water significantly decreased (P<0.001; P<0.004, P<0.001 respectively). There was no significant decrease in fat mass (P<0.061). Furthermore, IHG and IBS significantly decreased (P<0.001). DPC significantly altered with the left supporting leg in two positions of the right leg (posteromedial, P<0.038; posterior, P<0.012). At last, RPE significantly increased (P<0.001). CONCLUSION Previous studies showed that the rapid decline of body mass affects health and muscular and energetic performance while the present study highlights that it also alters perceived exertion and dynamic postural control.
Downregulation of BCL2 by miRNAs augments drug-induced apoptosis – a combined computational and experimental approach

A number of anti-cancer strategies aim to target the mitochondrial apoptotic machinery to induce tumour cell death. Mitochondria play a key role as death amplifiers by releasing apoptogenic factors from the mitochondrial inter-membrane space into the cytosol. BCL2 proteins are known for their ability to regulate both mitochondrial physiology and cell death, and their deregulated expression often renders cancer cells insensitive to apoptosis-inducing anticancer drugs. Recently, a few microRNAs, a novel class of gene regulators, have been demonstrated to regulate expression of some members of the BCL2 family. Here, we have combined computational and experimental approaches to identify miRNAs that can regulate the anti-apoptotic protein BCL2. We report that miR-195, miR-24-2 and miR-365-2 act as negative regulators of BCL2 through direct binding to their respective binding sites in the 3′-UTR of the human BCL2 gene. Ectopic expression of miR-195, miR-24-2 and miR-365-2 individually led to a significant reduction of the levels of BCL2 protein. Additionally, we found that overexpression of these miRNAs induced dissipation of the mitochondrial membrane potential and release of cytochrome c from mitochondria into the cytosol. Furthermore, we demonstrated that overexpression of these miRNAs not only caused an increase in apoptosis but also augmented the apoptotic effect of etoposide in breast cancer MCF7 cells. These data not only show the apoptotic nature of miR-195, miR-24-2 and miR-365-2 but also highlight the therapeutic potential of these miRNAs.
Taylor Rule Based Exchange Rate Models with Wealth Effects

This thesis focuses on the relationship between the exchange rate and its determinants using an endogenous monetary policy rule as represented by the Taylor rule. Compared to the recent literature on out-of-sample exchange rate predictability, I extend the model of Molodtsova and Papell (2009) by including two variables representing wealth effects, as has been suggested in the standard Taylor rule models. Using quarterly data from 1975-2008, I first investigate the econometric properties of the Taylor rule applied to U.K., Australian and Swedish data against the US dollar. Various unit root tests indicate that variables commonly used in such models are likely to be integrated of order one. However, by accounting for structural breaks, I can conclude that all variables are stationary. Parameter estimates suggest wealth effects are strongly related to the nominal exchange rates in these countries, in contrast to the standard monetary variables. Furthermore, I evaluate short-horizon exchange rate predictability with the Taylor rule fundamentals model for the U.S. dollar against the Australian dollar, Swedish Krona and British Pound. Following the recent literature, a robust set of out-of-sample statistics, including the Clark and West statistic, Diebold-Mariano statistics and Theil’s U ratio are used to evaluate the forecast performance. Current results from the Theil’s U ratio and CW statistics shows the Taylor rule incorporating the wealth effect improves the short run exchange rate forecast performance. Finally, we model the exchange rate from 1975 to 2008 as a Smooth Transition Regression (STR) based model in which a series of economically meaningful transition variables drive the movement across exchange rate regimes. The overall findings show strong evidence supporting the nonlinear relationship between the exchange rate and economic variables. Moreover, the STR Taylor rule models of the exchange rate substantially outperform both the random walk model and the linear Taylor rule model in forecasting the exchange rate.
Intratumoral lymphatics and lymph node metastases in papillary thyroid carcinoma.

OBJECTIVE To examine the relationship between lymphatic vessel density and clinical and pathological variables in patients with well-differentiated papillary thyroid carcinoma. SUBJECTS Clinical information was retrieved on 109 previously untreated patients with well-differentiated papillary thyroid carcinoma treated with total thyroidectomy and postoperative iodine I 131 ablation. Median follow-up was 38 months. DESIGN Archived tissue specimens were sectioned and stained with hematoxylin-eosin and anti-LYVE-1 antibody, a highly specific marker for lymphatic endothelium. The size of the tumor and its multifocality were noted and lymphatic vessel density was measured by means of Chalkley point counting. RESULTS Numerous intratumoral lymphatics were seen in papillary thyroid carcinoma. There was a highly significant association between the presence of intratumoral lymphatics and the presence of neck node metastases (P<.001). There was also a significant association with male sex (P =.03) and the presence of multifocal disease (P =.05). The presence of intratumoral lymphatics remained significantly associated with the presence of nodal metastases at presentation (P =.003) on multivariate analysis. Intratumoral lymphatics were not a significant predictor of tumor recurrence (P =.42, log-rank test). CONCLUSIONS The development of intratumoral lymphatics in well-differentiated papillary thyroid carcinoma appears to be associated with the spread of tumor to regional lymph nodes. The antimetastatic potential of targeting these lymphatics may be of potential therapeutic benefit in the future.
Thymosin Alpha 1 as an Adjunct to Influenza Vaccination in the Elderly

Abstract: From a clinical perspective, the immune deficiency of aging (immune senescence) is not profound. In fact, it may be of little clinical consequence. However, older people are prone to chronic and debilitating disorders which alone, or in concert with the medications used in their treatment, may add to the age effect and create a more clinically relevant immune deficiency. As a result, many older people are susceptible to infection. Furthermore, it is now well recognized that older people respond less well to immunization protocols. Protection against influenza by vaccination with hemagluttinin is the prototype example. Despite programs that have raised vaccination rates dramatically over the past three decades, influenza remains a major cause of morbidity and mortality in the elderly. This, in part, is due to the fact that vaccine responses are reduced in older recipients. Strategies are under development to enhance vaccine efficacy in this population and one such strategy is the adjuvant use of thymosin alpha 1 (Tα1). In both animal experiments and human trials, there has been demonstrated enhancement of vaccine responses. The findings to date warrant additional efforts to further examine the role of Tα1 in augmenting specific vaccine responses both in the elderly or in younger subjects in situations in which there are suboptimal quantities of immunizing antigen available.
Complexity: A Guided Tour

What enables individually simple insects like ants to act with such precision and purpose as a group? How do trillions of individual neurons produce something as extraordinarily complex as consciousness? What is it that guides self-organizing structures like the immune system, the World Wide Web, the global economy, and the human genome? These are just a few of the fascinating and elusive questions that the science of complexity seeks to answer. In this remarkably accessible and companionable book, leading complex systems scientist Melanie Mitchell provides an intimate, detailed tour of the sciences of complexity, a broad set of efforts that seek to explain how large-scale complex, organized, and adaptive behavior can emerge from simple interactions among myriad individuals. Comprehending such systems requires a wholly new approach, one that goes beyond traditional scientific reductionism and that re-maps long-standing disciplinary boundaries. Based on her work at the Santa Fe Institute and drawing on its interdisciplinary strategies, Mitchell brings clarity to the workings of complexity across a broad range of biological, technological, and social phenomena, seeking out the general principles or laws that apply to all of them. She explores as well the relationship between complexity and evolution, artificial intelligence, computation, genetics, information processing, and many other fields. Richly illustrated and vividly written, Complexity: A Guided Tour offers a comprehensive and eminently comprehensible overview of the ideas underlying complex systems science, the current research at the forefront of this field, and the prospects for the field's contribution to solving some of the most important scientific questions of our time.
An in vivo model for gastric physiological and pathophysiological studies in the mouse.

AIM In vivo models for studying gastrointestinal physiology and pathophysiology are well established in rats. Since a number of genetically modified mice are available there is a need for reliable mouse models. The aim of this project was to develop an in vivo mouse model for gastrointestinal studies. METHODS C57bl/6, NMRI and transgenic FVB/N (expressing human alpha-1,3/4-fucosyltransferase) mice were anaesthetized with isoflurane and the gastric mucosa exteriorized for intravital microscopy. Acid-base status and acid secretion were measured and blood pressure was continuously monitored. Gastric mucosal blood flow was recorded by laser-Doppler flowmetry. Mucus thickness and accumulation rate were measured with micropipettes. RESULTS We have developed an in vivo mouse model for studies of the gastric mucosa. With isoflurane anaesthesia the preparation can be studied for up to 5 h with stable blood pressure and mucosal blood flow. Acid-base status agrees with results from other laboratories. Blood flow increased in both C57bl/6 and alpha1.3/4-FT mice in response to luminal HCl, and the mucus gel could be divided into a firmly and a loosely adherent layer, all comparable with results in the rat. However, the firmly adherent mucus layer was thinner (45 +/- 2 microm), and the mucus accumulation rate lower, than in the rat. Furthermore, both basal and stimulated acid secretion showed lower outputs than in the rat. CONCLUSIONS This model has great potential for investigations of gastrointestinal physiology and pathophysiology and can be applied for Helicobacter pylori infection studies.
Differential contribution of afferent and central pathways to the development of baroreflex dysfunction in chronic kidney disease

The effects of chronic kidney disease on baroreflex control of renal sympathetic nerve activity (RSNA) and deficits in afferent and central components of the baroreflex were studied in juvenile and adult male Lewis Polycystic Kidney (LPK) and control Lewis rats under anesthesia (n=35). Blood pressure (BP), heart rate (HR), aortic depressor nerve activity (ADNA), and RSNA were determined after pharmacological manipulation of BP. Responses to ADN stimulation (4.0 V, 2.0 ms, 1–24 Hz) were determined, and the aortic arch was collected for histomorphometry. In juvenile LPK versus age-matched Lewis rats, gain of RSNA (−1.5±0.2 versus −2.8±0.2%/mm Hg; P<0.05) and ADNA (2.5±0.3 versus 5.0±0.6%/mm Hg; P<0.05), but not HR barocurves, were reduced. BP, HR, and RSNA responses to ADN stimulation were normal or enhanced in juvenile LPK. In adult LPK versus age-matched Lewis, the gain and range of RSNA (gain: −1.2±0.1 versus −2.2±0.2%/mm Hg, range: 62±8 versus 98±7%) and HR (gain: −0.7±0.1 versus −3.5±0.7 bpm/mm Hg, range: 44±8 versus 111±19 bpm) barocurves were reduced (P<0.05). The gain and range of the ADNA barocurves were also reduced in adult LPK versus Lewis [1.5±0.4 versus 5.2±1.1 (%/mm Hg) and 133±35 versus 365±61 (%) P<0.05] and correlated with aortic arch vascular remodeling. BP, HR, and RSNA responses to ADN stimulation were significantly reduced in adult LPK. Our data demonstrate a deficit in the afferent component of the baroreflex that precedes the development of impaired central regulation of RSNA and HR in chronic kidney disease, and that progressive impairment of both components is associated with marked dysfunction of the baroreflex pathway.
Does delayed gastric emptying really cause symptoms in functional dyspepsia? We still doubt it!

We enjoyed reading the provocative commentary by Camilleri ( Gut 2006; 55 :909–10) on our large study of patients with functional dyspepsia ( Gut 2006; 55 :933–9). We completely agree that delayed gastric emptying is a marker of disturbed pathophysiology in functional dyspepsia; indeed, we first reported this observation in 1989.1 However, we remain unconvinced, based on the available data, that this abnormality alone is linked to upper gastrointestinal symptoms.1–3 Factor analysis studies from the general population, in the absence of objective testing, do not provide insights into this issue,4,5 although we have shown that non-consulters with dysmotility-like dyspepsia are more likely to have gastric emptying delay.6 Studies from selected tertiary care patients are of interest, but Camilleri has previously reported negative results.3 Importantly, in a previous study of 551 patients with functional dyspepsia and 247 patients with type I diabetes and postprandial dyspepsia, gastric emptying, as measured by C13 octanoic acid breath testing, was …
Risk-On/Risk-Off: Financial Market Response to Investor Fear

This paper examines the relationship between changes in the level of investor fear (measured by VIX) and financial market returns. We document a statistically significant relationship, across asset classes, consistent with a flight to quality as investor fear increases. As VIX increase there is a decline in stock markets, bond yields, and high-yielding currencies (AUD and NZD), while the USD appreciates. Returns become more sensitive to changes in the level of investor fear during the financial crisis of 2008–09, when investor fear spikes sharply. Analysis of market returns subsequent to periods of extreme levels of investor fear suggests some predictive ability for future returns, and it is suggested that this may be used to develop a profitable trading strategy. Taken together, the results confirm that financial market returns are closely related to prevailing levels of investor fear.
Differences in the Expression of Human Class I MHC Alleles and Their Associated Peptides in the Presence of Proteasome Inhibitors1

We have studied the contributions of proteasome inhibitor-sensitive and -insensitive proteases to the generation of class I MHC-associated peptides. The cell surface expression of 13 different human class I MHC alleles was inhibited by as much as 90% or as little as 40% when cells were incubated with saturating concentrations of three different proteasome inhibitors. Inhibitor-resistant class I MHC expression was not due to TAP-independent expression or preexisting internal stores of peptides. Furthermore, it did not correlate with the amount or specificity of residual proteasome activity as determined in in vitro proteolysis assays and was not augmented by simultaneous incubation with multiple inhibitors. Mass spectrometry was used to directly characterize the peptides expressed in the presence and absence of proteasome inhibitors. The number of peptide species detected correlated with the levels of class I detected by flow cytometry. Thus, for many alleles, a significant proportion of associated peptide species continue to be generated in the presence of saturating levels of proteasome inhibitors. Comparison of the peptide-binding motifs of inhibitor-sensitive and -resistant class I alleles further suggested that inhibitor-resistant proteolytic activities display a wide diversity of cleavage specificities, including a trypsin-like activity. Sequence analysis demonstrated that inhibitor-resistant peptides contain diverse carboxyl termini and are derived from protein substrates dispersed throughout the cell. The possible contributions of inhibitor-resistant proteasome activities and nonproteasomal proteases residing in the cytosol to the peptide profiles associated with many class I MHC alleles are discussed.
Identification and molecular characterization of the gene coding for acetaldehyde dehydrogenase II (acoD) of Alcaligenes eutrophus

The N-terminal amino acid sequence of purified acetaldehyde dehydrogenase II (AcDH-II) from ethanol-grown cells of Alcaligenes eutrophus was determined. By using oligonucleotides deduced from this sequence the structural gene for AcDH-II, which was referred to as acoD, was localized on a 7.2-kbp EcoRI restriction fragment (fragment D), which has been cloned recently (C. Fründ, H. Priefert, A. Steinbüchel, and H. G. Schlegel, J. Bacteriol. 171:6539-6548, 1989). A 2.8-kbp PstI subfragment of D, which harbored acoD, was sequenced. It revealed an open reading frame of 1,518 bp, encoding a protein with a relative molecular weight of 54,819. The insertions of Tn5::mob of two transposon-induced mutants of A. eutrophus, which were impaired in the catabolism of acetoin, were mapped 483 or 1,359 bp downstream from the translational start codon of acoD. The structural gene was preceded by a putative Shine-Dalgarno sequence. The transcriptional start site 57 bp upstream of acoD was identified and was preceded by a sequence which exhibited a striking homology to the enterobacterial sigma 54-dependent promoter consensus sequence. This was in accordance with the observation that the expression of acoD and of other acetoin-catabolic genes depended on the presence of an intact rpoN-like gene. Alignments of the amino acid sequence deduced from acoD with the primary structures of aldehyde dehydrogenases from other sources revealed high degrees of homology, amounting to 46.5% identical amino acids.
Long‐term treatment with methylphenidate for fatigue after traumatic brain injury

Traumatic brain injury (TBI) may cause long‐lasting post‐concussive symptoms, such as mental fatigue and concentration difficulties, and this may become the main hindrance for returning to work and studies. There is currently no effective treatment for long‐lasting mental fatigue. In this hypothesis generating study, the long‐term effects of methylphenidate on mental fatigue, cognitive function, and safety were assessed.
A comparison of the typical features of chikungunya infection internationally

A 22-year-old university undergraduate presented with persistent fever and appearance of rash on the 4th day of illness. On the 3rd day, he consulted his general practitioner (GP) who detected thrombocytopenia. The dengue duo test (dengue NS1 antigen, IgM and IgG) was negative. Concerned after the rash appeared, the patient sought consultation at the Emergency Department (ED) in a local hospital and was admitted. Investigations in hospital confirmed chikungunya infection. This case report highlights two key messages in the American Centers for Disease Control and Prevention (CDC) advisory: (1) it is difficult to distinguish chikungunya and dengue based on clinical findings alone; (2) the patient should be managed as having dengue until dengue has been excluded.