Miracle-dz/UniFAR-FTUs huggingface dataset:
Four factors of change: adaptations of everyday design

This paper is a follow up study of a 2005-2006 study of everyday design. This follow-up study is an opportunity to gain insights into the social evolution of everyday design systems in the home. We report on changes to five systems and discuss how these changes occurred over the last four to five years. We identify four factors related to the changes 1) shared intent 2) mutual intelligibility, 3) materiality-substitutability, and 4) fit.
Predictors of quality of life in major psychoses: a naturalistic follow-up study.

BACKGROUND Improved quality of life (QOL) of patients suffering from major psychoses has become an important treatment goal. We sought to determine predictors of perceived QOL and to explore the changes that occur regarding QOL among individuals with schizophrenia as compared to patients with schizoaffective/mood disorders. METHOD In a naturalistic longitudinal design, 148 inpatients with schizophrenia and 51 inpatients with schizoaffective/mood disorders (DSM-IV) were tracked for 16 months (SD = 4.6 months). Subjects were assessed at 2 timepoints for psychopathology, stress process-related factors, and perceived QOL, as measured by the Quality of Life Enjoyment and Satisfaction Questionnaire. Predictors of fluctuations in QOL index scores during the follow-up period were identified using multiple regression techniques. RESULTS We found that poor QOL is not a more severe problem for schizophrenia patients than for schizoaffective/mood disorder patients. Improved QOL of schizophrenia patients is associated with reduced paranoid and distress (obsessiveness, somatization) symptoms and increased self-efficacy and self-esteem ratings. Individual changes in QOL index scores among patients with schizoaffective/mood disorders are associated with changes in depression, sensitivity, expressed emotion, and task-oriented coping scores. CONCLUSION Predictors of changes in satisfaction with life quality over time among schizophrenia patients are distinct from those associated with schizoaffective/mood disorders. Changes in stress process-related factors, rather than psychopathology, predict change in perceived QOL and should be considered when evaluating QOL outcomes.
Oral bile acid treatment and the patient with zellweger syndrome

The cerebrohepatorenal syndrome of Zellweger is a congenital syndrome of multiple manifestations, including hepatomegaly and liver dysfunction. Treatment is generally of a supportive nature, aimed at improving nutrition and growth, controlling the central nervous system symptoms and limiting progression of liver disease. Because the liver disease in Zellweger syndrome may be attributed to an overproduction and accumulation of cholestanoic acids, exacerbated by diminished primary bile acid synthesis, we hypothesized that primary bile acid administration would be beneficial in improving liver function by a mechanism involving down‐regulation in the synthesis of these atypical bile acids. We report here the clinical and biochemical responses to primary bile acid administration in a 2‐mo‐old boy who was seen with the typical signs of Zellweger syndrome. Liver disease was evident from hepatomegaly and elevated serum liver enzymes and bilirubin. The diagnosis was supported by markedly elevated serum very long chain fatty acids and the bile acids dihydroxycholestanoic acid and trihydroxycholestanoic acid. Confirmation of the lack of peroxisomes was established by electron microscopy. When the patient was 6 mo old, the primary bile acids cholic acid and chenodeoxycholic acid, (100 mg each/day) were administered orally. A significant improvement in biochemical indices of liver function occurred with a normalization of the serum bilirubin and liver enzymes and a histological improvement in the extent of inflammation and bile duct proliferation and disappearance of cannalicular plugs. Serum and urinary cholestanoic acids showed a significant decrease within a few days. A striking and sustained increase in growth was observed after therapy, and an improvement in neurological symptoms was noted. In conclusion, this study indicates that primary bile acid therapy improves liver function and growth in the patient with peroxisomal dysfunction and should be considered in the supportive therapies for this condition. (Hepatology 1992;15:198‐207).
Evidence for BCR‐ABL‐dependent dysfunctions of iNKT cells from chronic myeloid leukemia patients

Chronic myeloid leukemia (CML) is a clonal hematopoietic stem‐cell malignancy characterized by the presence of the chimeric BCR‐ABL oncoprotein with deregulated tyrosine‐kinase (TK) activity. Although conventional T cells are acknowledged as important players in the control of CML, a possible modification of invariant NKT (iNKT) cells, known for their antitumoral activity, has not been established as yet. Here, we showed that the expression of perforin, CD95L, and promyelocytic leukemia zinc finger, a transcription factor required for maintenance of iNKT cell functions, was reduced or suppressed in CML patients at diagnosis, as compared with healthy individuals. The proliferation rate of blood iNKT cells in response to their cognate ligand was likewise diminished. These functional deficiencies were corrected in patients having achieved complete cytogenetic remission following TK inhibitor or IFN‐α therapy. iNKT cells from CML patients in the chronic phase did not display increased TK activity, which argued against a direct autonomous action of BCR‐ABL. Instead, we found that their anergic status originated from both intrinsic and APC‐dependent dysfunctions. Our data demonstrate that chronic phase CML is associated with functional deficiencies of iNKT cells that are restored upon remission. These results suggest a possible contribution to disease control by TK inhibitor therapies.
Regulation of meiosis during mammalian spermatogenesis: the A-type cyclins and their associated cyclin-dependent kinases are differentially expressed in the germ-cell lineage.

To begin to examine the function of the A-type cyclins during meiosis in the male, we have examined the developmental and cellular distribution of the cyclin A1 and cyclin A2 proteins, as well as their candidate cyclin-dependent kinase partners, Cdk1 and Cdk2, in the spermatogenic lineage. Immunohistochemical localization revealed that cyclin A1 is present only in male germ cells just prior to or during the first, but not the second, meiotic division. By contrast, cyclin A2 was expressed in spermatogonia and was most abundant in preleptotene spermatocytes, cells which will enter the meiotic pathway. Immunohistochemical detection of Cdk1 was most apparent in early pachytene spermatocytes, while staining intensity diminished in diplotene and meiotically dividing spermatocytes, the cells in which cyclin A1 expression was strongest. Cdk2 was highly expressed in all spermatocytes. Notably, in cells undergoing the meiotic reduction divisions, Cdk2 appeared to localize specifically to the chromatin. This was not the case for spermatogonia undergoing mitotic divisions. In the testis, cyclin A1 has been shown to bind both Cdk1 and Cdk2 but we show here that cyclin A2 binds only Cdk2. These results indicate that the A-type cyclins and their associated kinases have different functions in the initiation and passage of male germ cells through meiosis.
Prognosis of Depression in the Elderly

The prognosis of depression in the elderly was investigated in a mixed-age sample of 242 consecutive referrals, with DSM-III defined unipolar major depressive episode, to a specialist unit for mood disorders. Subjects were followed up at about 1 and 3.8 years. There was no significant difference in outcome between younger (under 40 years), middle aged (40–59 years) and older (60 years or more) depressed patients. For the 61 elderly subjects with depression, prognosis improved with time, with 25% having a lasting recovery at the first and 41% at the second follow-up. Early onset, recurrence, and poor premorbid personality were associated with a worse prognosis. Three (5%) elderly depressives had committed suicide and seven (11%) had died from natural causes by the second follow-up. Despite some methodological limitations, our findings suggest a more optimistic outlook and the need for longer, more assertive treatment for elderly, depressed patients.
Controlling Intentions

Decades of cognitive-control research have highlighted the difficulty of controlling a prepotent response. We examined whether having prepotent prospective-memory intentions similarly heightens the difficulty associated with stopping an intention once a prospective-memory task is finished. In three experiments, participants encoded a prospective-memory intention (e.g., press Q in response to the targets corn and dancer) and subsequently encountered either four targets or zero targets. Instructions then indicated that the prospective-memory task was finished. In a follow-up task, the targets appeared, and commission errors were recorded. Surprisingly, it was easier for participants to stop the intention when it had been fulfilled (four-target condition) than when it had gone unfulfilled (zero-target condition; Experiments 1 and 2). This was true even after intention cancellation (Experiment 2). Although repeatedly performing an intention strengthens target-action links, it appears to enable deactivation of the intention, a process that is largely target specific (Experiment 3). We relate these findings to the Zeigarnik effect, target-action deactivation, and reconsolidation theories.
Digital Predistortion for Power Amplifier Based on Sparse Bayesian Learning

In this brief, a sparse-Bayesian-learning algorithm is applied to estimate the coefficients of the power amplifier (PA) behavioral models and inverse models from the view of probability. With this sparse learning method, the needed number of samplings can be reduced significantly. In addition, it also provides researchers with ideas that obtain the needed subspace of the preselected model. The performance of the algorithm is validated experimentally on a gallium nitride (GaN) PA, and the signal used to test the proposed approach is an Long Term Evolution (LTE) signal. A comparison with the state-of-the-art estimation algorithm in an open-loop digital-predistortion system is also presented, and the vast majority of tests show that the number of model coefficients is reduced by at least 50%.
Valganciclovir Results in Improved Oral Absorption of Ganciclovir in Liver Transplant Recipients

ABSTRACT The pharmacokinetics of an orally administered valine ester of ganciclovir (GCV), valganciclovir (VGC), were studied. These were compared to the pharmacokinetics of oral and intravenous GCV. Twenty-eight liver transplant recipients received, in an open-label random order with a 3- to 7-day washout, each of the following: 1 g of oral GCV three times a day; 450 mg of VGC per os (p.o.) once a day (q.d.); 900 mg of VGC p.o. q.d. ; and 5 mg of intravenous (i.v.) GCV per kg of body weight q.d. , given over 1 h. GCV and VGC concentrations were measured in blood over 24 h. One-sided equivalence testing was performed to test for noninferiority of 450 mg of VGC relative to oral GCV (two-sided 90% confidence interval [CI] > 80%) and nonsuperiority of 900 mg of VGC relative to i.v. GCV (two-sided 90% CI < 125%). The exposure of 450 mg of VGC (20.56 μg · h/ml) was found to be noninferior to that of oral GCV (20.15 μg · h/ml; 90% CI for relative bioavailability of 95 to 109%), and the exposure of 900 mg of VGC (42.69 μg · h/ml) was found to be nonsuperior to that of i.v. GCV (47.61 μg · h/ml; 90% CI = 83 to 97%). Oral VGC delivers systemic GCV exposure equivalent to that of standard oral GCV (at 450 mg) or i.v. GCV (at 900 mg of VGC). VGC has promise for effective CMV prophylaxis or treatment with once-daily oral dosing in transplant recipients.
Estimation of polymeric IgA in human serum: an assay based on binding of radiolabeled human secretory component with applications in the study of IgA nephropathy, IgA monoclonal gammopathy, and liver disease.

Binding of 125I-human secretory component (SC) to human polymeric immunoglobulin A (pIgA) was employed to measure quantitatively the pIgA present in human sera. Interference by IgM in some sera was prevented by removal of IgM with glutaraldehyde polymerized anti-IgM antibodies. 125I-SC complexed to pIgA was measured by precipitation with anti-IgA antibodies and the quantity of pIgA in human serum was estimated by comparing the quantity of 125I-SC bound by several dilutions of human serum to that bound by standard quantities of human monoclonal pIgA proteins. The assay was specific for pIgA because heat-aggregated monomeric IgA or hypogammaglobulinemic serum did not bind 125I-SC greater than a precipitate formed with human monoclonal IgG and anti-IgG. Moreover, analysis of a series of IgA myeloma sera indicated no correlation between the IgA content of the serum and the quantity of pIgA measured. The quantity of pIgA found in 30 normal human sera was 0.13 +/- 0.08 mg/ml (1S.D.), which consisted of 11.3 +/- 5.3% (1 SD) of the total IgA. Patients with IgA monoclonal gammopathy were most often found to have predominantly monomeric IgA. Patients with IgA nephropathy also showed an elevation of pIgA, but this appeared to be a consequence of an overt IgA elevation. IgA nephropathy patients with elevated serum IgA in fact showed a significant elevation of monomeric IgA. Selective elevation of pIgA was observed in patients with primary biliary cirrhosis and alcoholic liver disease. A comparison of this assay with other assays to measure pIgA is discussed.
Liver regeneration in heparin-binding EGF-like growth factor transgenic mice after partial hepatectomy.

BACKGROUND & AIMS Heparin-binding epidermal growth factor-like growth factor (HB-EGF), a member of the EGF family, is synthesized in the form of a membrane-anchored precursor (proHB-EGF), which subsequently is processed proteolytically to mature HB-EGF. This study describes the effects of HB-EGF on liver regeneration after 70% partial hepatectomy in proHB-EGF transgenic mice with liver-specific expression. METHODS & RESULTS No significant differences in liver/body weight ratios and in bromodeoxyuridine (BrdU)-labeling index (the ratios of BrdU-positive hepatocyte nuclei) were found between adult transgenic and wild-type mice. However, in regenerating liver after partial hepatectomy, transgenic mice had higher liver/body weight ratios than wild-type mice and at 120 hours reached a level equal to that before partial hepatectomy. The BrdU-labeling index was about 5 times higher in the livers of transgenic mice compared with the wild type (51.5% vs. 10.2%, respectively; P < 0.01) at 48 hours after partial hepatectomy. Activation of microtubule-associated protein kinase after partial hepatectomy was higher and earlier in the transgenic mice as compared with the wild-type mice. Soluble HB-EGF was increased in the liver (at 8 min) after partial hepatectomy, indicating that the shedding of proHB-EGF occurred after partial hepatectomy. CONCLUSIONS The transgenic expression of HB-EGF accelerates the proliferation of hepatocytes after partial hepatectomy, suggesting that HB-EGF functions as a hepatotrophic factor in vivo.
H‐hernioplasty: A tension‐free repair for umbilical hernia

Tension-free repair of inguinal and incisional hernias is now frequently performed using mesh prostheses. Umbilical hernias can also benefit from this approach, although positioning of the mesh may be difficult owing to the often small diameter of the defect. Preliminary results are presented of a technique that uses a polypropylene mesh prosthesis to repair umbilical hernias and fulfils the principles of mesh hernioplasty without having to enlarge the defect.
The Stanwick Villa, Northants: An Interim Report on the Excavations of 1984–88

The Roman villa at Stanwick (GR SP 972716) is situated on the west side of Stanwick village and the newly constructed A405 bypass. It occupies a gravel terrace on the east bank of the River Nene close to a point where the river swings west to join a secondary canalized channel on the west side of the floodplain. The area immediately west of the villa was partially disturbed in 1845 by the construction of an embankment for the now disused Blisworth-Peterborough railway. The south side of the site is bounded by a stream which rises as a spring east of the village: other springs issue from the valley slope close to the villa where the gravels give way to a bedrock of clay and cornbrash, a decomposed oolitic limestone. Beds of limestone occupy the higher slopes and were quarried in Roman and medieval times. Both the availability of fresh water and of building-stone probably influenced the location of the site.
Trade-offs Drive the Evolution of Increased Complexity in Nascent Multicellular Digital Organisms

The transition to multicellularity was a major step in the evolution of large, complex life on Earth (Maynard Smith and Szathmáry 1995). Unlike other major evolutionary transitions, which have occurred only once (e.g., prokaryotes to eukaryotes), multicellularity has evolved multiple times in diverse lineages including archaea (Jahn et al. 2008), bacteria (Velicer and Vos 2009; Overmann 2010; Schirrmeister et al. 2011), and eukaryotes (Bonner 1998; King 2004; Grosberg and Strathmann 2007; Herron et al. 2013). Prior work suggests that the formation of simple clusters of cells, the first step in the transition to multicellularity, may be adaptive under a number of distinct ecological scenarios. For example, clusters may provide protection from predation (Kessin et al. 1996; Boraas et al. 1998), protection from environmental stress (Smukalla et al. 2008), or improved utilization of diffusible nutrients (Pfeiffer and Bonhoeffer 2003, Koschwanez et al. 2011; Koschwanez et al. 2013). Nevertheless, how and why nascent multicellular lineages evolve increased complexity remains a fundamental question in evolutionary biology. Progress has been impeded by a lack of experimental systems due to the fact that most nascent multicellular lineages have been lost to extinction.
Attention-Deﬁcit/Hyperactivity Disorder in a Population Isolate: Linkage to Loci at 4q13.2, 5q33.3, 11q22, and 17p11

Attention-deﬁcit/hyperactivity disorder (ADHD [MIM 143465]) is the most common behavioral disorder of childhood. Twin, adoption, segregation, association, and linkage studies have conﬁrmed that genetics plays a major role in conferring susceptibility to ADHD. We applied model-based and model-free linkage analyses, as well as the pedigree disequilibrium test, to the results of a genomewide scan of extended and multigenerational families with ADHD from a genetic isolate. In these families, ADHD is highly comorbid with conduct and oppositional deﬁant disorders, as well as with alcohol and tobacco dependence. We found evidence of linkage to markers at chromosomes 4q13.2, 5q33.3, 8q11.23, 11q22, and 17p11 in individual families. Fine mapping applied to these regions resulted in signiﬁcant linkage in the combined families at chromosomes 4q13.2 (two-point allele-sharing LOD score from LODPAL p 4.44 at D4S3248 ), 5q33.3 (two-point allele-sharing LOD score from LODPAL p 8.22 at D5S490 ), 11q22 (two-point allele-sharing LOD score from LODPAL p 5.77 at D11S1998 ; multipoint nonparametric linkage [NPL] 5 log [ P value] p 5.49 at ∼ 128 cM), and 17p11 (multipoint NPL 5 log [ P value] 1 12 at ∼ 12 cM; multipoint maximum location score 2.48 [ a p 0.10] at ∼ 12 cM; two-point allele-sharing LOD score from LODPAL p 3.73 at D17S1159 ). Additionally, suggestive linkage was found at chromosome 8q11.23 (combined two-point NPL 5 log [ P value] 1 3.0 at D8S2332 ). Several of these regions are novel (4q13.2, 5q33.3, and 8q11.23), whereas others replicate already-published loci (11q22 and 17p11). The concordance between results from different analytical methods of linkage and the replication of data between two independent studies suggest that these loci truly harbor ADHD susceptibility genes.
Phenotypic Modulation of Vascular Smooth Muscle Cells Induced by Unsaturated Lysophosphatidic Acids

Abstract— The phenotypic modulation of vascular smooth muscle cells (VSMCs) from the differentiated state to the dedifferentiated one is critically involved in the development and progression of atherosclerosis. Although many cytokines and growth factors have been reported as atherogenic factors, the critical pathogens for inducing atherosclerosis remain unknown, largely because proper examining systems of them have not been developed. We recently established primary culture systems for visceral SMCs and VSMCs in which both SMCs, when cultured on laminin with insulin-like growth factor-I, show a differentiated phenotype, as indicated by a spindle-like shape, ligand-induced contractility, and a high level of SMC differentiation marker gene expression. In this study, we searched for critical dedifferentiation factors for these SMCs using our culture system. We found that polar lipids extracted from human serum markedly induced VSMC dedifferentiation, and this activity was solely present in the lysophosphatidic acid (LPA) fraction. Among several LPA species detected in human serum lipids, unsaturated LPAs were identified as major contributors to the induction of VSMC dedifferentiation. Signaling and phenotype analyses revealed that unsaturated LPA–induced VSMC dedifferentiation is mediated through the coordinated activation of extracellular signal–regulated kinase and p38 mitogen–activated protein kinase. Thus, this report demonstrates the first finding that unsaturated LPAs, but not saturated LPAs, specifically induce VSMC phenotypic modulation, suggesting that these molecules could function as atherogenic factors.
MORPHOLOGICAL DIVERGENCE OF BREEDERS AND HELPERS IN WILD DAMARALAND MOLE‐RAT SOCIETIES

The specialization of body shape to an individual's role within society represents a pinnacle of social evolution. Although commonplace among social insects, divergence in the body shapes of breeders and helpers has to date been documented in just one social vertebrate, the naked mole‐rat, Heterocephalus glaber; an extraordinary species in which large colony size and frequent inbreeding may have favored the evolution of such specialization. Here, we present new evidence of morphological divergence between breeders and helpers in the Damaraland mole‐rat, Fukomys damarensis; a much less socially extreme species that reflects an independent evolutionary origin of sociality. Using longitudinal data from wild populations, we show that dominant female Damaraland mole‐rats, like many social insect queens, have a significantly more elongate body shape than subordinates. This difference arises not from a pre‐existing difference in the body shapes of subordinates that do, and those that do not, become dominant, but from a modification to the growth trajectory of subordinates on dominance acquisition. Our findings reveal a wider role for morphological divergence within vertebrate societies and, as Damaraland mole‐rats neither live in unusually large groups nor inbreed, suggest that circumstances favoring the evolution of such specializations may be more widespread among vertebrates than previously supposed.