Miracle-dz/UniFAR-FTUs huggingface dataset:
Dialysis Patients Refusing Kidney Transplantation: Data From the Slovenian Renal Replacement Therapy Registry

Kidney transplantation is considered the best renal replacement therapy (RRT) for patients with end‐stage renal disease; nevertheless, some dialysis patients refuse to be transplanted. The aim of our registry‐based, cross‐sectional study was to compare kidney transplant candidates to dialysis patients refusing transplantation. Data were collected from the Slovenian Renal Replacement Therapy Registry database, as of 31 December 2008. Demographic and some RRT data were compared between the groups. There were 1448 dialysis patients, of whom 1343 were treated by hemodialysis and 105 by peritoneal dialysis (PD); 132 (9%) were on the waiting list for transplantation, 208 (14%) were preparing for enrollment (altogether 340 [23%] dialysis patients were kidney transplant candidates); 200 (13.7%) patients were reported to refuse transplantation, all ≤65 years of age; 345 (24%) were not enrolled due to medical contraindications, 482 (33%) due to age, and 82 (6%) due to other or unknown reasons. No significant difference was found in age, gender, or presence of diabetes between kidney transplant candidates vs. patients refusing transplantation (mean age 50.5 ± 13.9 vs. 51.3 ± 9.6 years, males 61% vs. 63%, diabetics 18% vs. 17%). The proportion of patients ≤ 65 years old who were refusing transplantation was 28% (187/661) for hemodialysis and 17% (13/79) for PD patients (P = 0.03). There is a considerable group of dialysis patients in Slovenia refusing kidney transplantation. Compared to the kidney transplant candidates, they are similar in age, gender and prevalence of diabetes. Patients treated by peritoneal dialysis refuse kidney transplantation less often than hemodialysis patients.
Correlation with changes in horns and pelage, but not reproduction, of seasonal cycles in the secretion of prolactin in rams of wild, feral and domesticated breeds of sheep.

Seasonal cycles were monitored in groups of wild (mouflon), feral (Soay) and domesticated breeds of sheep (Shetland, Blackface, Herdwick, Norfolk, Wiltshire, Portland, Merino, Soay x Portland and Soay x Merino) living outdoors near Edinburgh (56 degrees N). Changes in the blood plasma concentrations of prolactin and FSH, and growth of the horns and pelage were measured every half calendar month from 1 to 3 years of age. In all breeds there was a clearly defined seasonal cycle in the plasma concentration of prolactin with an 18-66-fold increase in mean values from the nadir in November and December to the peak in May and June. The seasonal increase in prolactin was closely correlated with the seasonal increase in the growth of the horns, both within and between breeds (e.g. time of peak prolactin vs horn growth for 11 breeds, R = 0.62, P less than 0.05). In the mouflon, Soay and some of the domesticated breeds of sheep (Wiltshire, Herdwick and Shetland), the seasonal increase in prolactin was also temporally correlated with the resurgence of growth of the pelage in spring and a conspicuous moult. In the other breeds developed to produce fine wool (e.g. Norfolk, Portland and Merino), there was no clear seasonal change in the pelage and growth continued throughout the year. Comparison between breeds indicated that continuous growth of the pelage was associated with higher plasma prolactin concentrations in winter. The times of the seasonal changes in plasma concentrations of prolactin were not significantly correlated with the corresponding changes in the plasma concentrations of FSH. The overall results are consistent with a role for prolactin related to the growth of the horns and pelage rather than the seasonal cycle in reproduction. The differences between the wild-type and the domesticated breeds in the pelage represent the effect of selective breeding to produce a long fine fleece which has involved changes in both the seasonal pattern of prolactin secretion and the growth characteristics of the hair fibres.
We know that MEMS is replacing quartz. But why? And why now?

MEMS (Microelectromechanical) oscillators were first introduced commercially six years ago. Now MEMS is making significant incursions into what was once the exclusive territory of quartz oscillators. Why is this transition happening now, rather than ten years ago or ten years from now? The transition has been paced by the MEMS community developing the necessary high stability, high frequency, high Q, and high output resonators. Also, MEMS oscillators rely on advanced circuit architectures, particularly leveraging fractional-PLLs and precision temperature sensors. These specialized circuits have only recently become sufficiently small, low noise, power efficient, and accurate.
Use of Truquant BR radioimmunoassay for early detection of breast cancer recurrence in patients with stage II and stage III disease.

PURPOSE The Truquant BR radioimmunoassay (RIA) (Biomira Diagnostics Inc, Rexdale, Canada) uses the monoclonal antibody B27.29 to quantitate the MUC-1 gene product (CA 27.29 antigen) in serum. We evaluated CA 27.29 antigen in a controlled, prospective clinical trial for its ability to predict relapse in stage II and stage III breast cancer patients. PATIENTS AND METHODS Over a 2-year period, 166 patients who had completed therapy for stage II (80.1%) or III (19.9%) breast cancer and were clinically free of disease were serially tested for CA 27.29 antigen levels. The study was double-masked and cancer recurrence was documented based on clinical findings. Patients with two consecutive CA 27.29 antigen test results above the upper limit of normal were considered positive. RESULTS The Truquant BR RIA had a sensitivity of 57.7%, specificity of 97.9%, positive predictive value of 83.3%, and negative predictive value of 92.6%. The recurrence rate was 15.7%. A Cox regression analysis showed that the only variable to correlate with recurrent disease was the CA 27.29 antigen test result. Patients with a positive test result had increased odds of having a recurrence (odds ratio, 6.8; P < .00001). The test was effective in predicting recurrence in patients with both distant and locoregional disease. In a subgroup of patients with bone pain, CA 27.29 antigen level was found to identify reliably patients who would subsequently develop recurrent disease. CONCLUSION These data demonstrate that the Truquant BR RIA can be used as an aid to predict recurrent breast cancer in patients with stage II and III disease.
Bile acids induce mitochondrial ROS, which promote activation of receptor tyrosine kinases and signaling pathways in rat hepatocytes

Previous studies have demonstrated in hepatocytes that deoxycholic acid (DCA) promotes inactivation of protein tyrosine phosphatases (PTPases) and activation of ERBB1 and the extracellular‐regulated kinase (ERK) 1/2 pathway. The present studies have determined the biochemical mechanism(s) through which these events occur. DCA and taurodeoxycholic acid (TDCA) (100 μmol/L) caused activation of ERBB1, insulin receptor, and the ERK1/2 and AKT pathways in primary rodent hepatocytes. DCA‐ and TDCA‐induced receptor and signaling pathway activations were blocked by the reactive oxygen species (ROS) scavengers N‐acetyl cysteine (NAC) and Trolox (TX), as well as by cyclosporin A (CsA) and bongkrekic acid (BKA). DCA activated the ERK1/2 pathway in HuH7 human hepatoma cells that was blocked by the incubation of cells with an ERBB1 inhibitor, NAC, TX, CsA, or BKA. DCA did not activate the ERK1/2 pathway in mitochondria‐defective HuH7 Rho 0 cells. In HuH7 cells and primary hepatocytes, DCA enhanced the production of ROS, an effect that was abolished in Rho 0 cells and by prior incubation of cells with CsA or BKA. In hepatocytes and HuH7 cells, DCA inhibited PTPase activity. Incubation of hepatocytes with either CsA or BKA prevented DCA‐induced inhibition of PTPase activity. Loss of mitochondrial function in Rho 0 cells also abolished the inhibitory effects of DCA on PTPase activity. In conclusion, DCA and TDCA cause ROS generation in hepatocytes that is dependent on metabolically active mitochondria. The generation of ROS is essential for PTPase inactivation, receptor tyrosine kinase activation, and enhanced signaling down the ERK1/2 and AKT pathways. (Hepatology 2004;40:961–971).
24-Hour Dialysate Collection for Determination of Peritoneal Membrane Transport Characteristics: Longitudinal Follow-Up Data for the Dialysis Adequacy and Transport Test (Datt)

Objective To determine the ability of the dialysis adequacy and transport test (DATT) to monitor changes in peritoneal transport characteristics over time. Setting University-based peritoneal dialysis program. Patients One hundred patients on continuous ambulatory peritoneal dialysis who underwent 226 simultaneous DATTs and peritoneal equilibration tests (PET). Methods Retrospective analysis of DA TT and PET data. Results The mean 24-hour dialysate-to-plasma creatinine (cr) concentration ratio (DIP cr) from the DATT was 0.70±0.10, and the mean four-hour DIP crfrorn the PET was 0.68 ± 0.10. The correlation coefficient between the fourhour and 24-hour DIP cr was 0.81, and the standard error of estimate was 0.065. The mean (±SD) difference between the four-hour and 24-hour DIP cr was 0.023 ± 0.061. Fifty eight patients had two or more sequential DA TTs and PETs. For these 94sets of sequential DATTs and PETs, the mean (±SD) difference between the change in the four-hour DIP cr and the change in the 24-hour DIP cr was 0.020 ± 0.024, and the standard error of estimate was 0.064. In 17 patients a change in dwell volume from 2.0 L to 2.5 L occurred between the first and second measures of peritoneal membrane transport characteristics. The mean (±SD) difference between the change in the four-hour DIP cr and the change in the 24-hour DIP cr was 0.036 ± 0.055, and the standard error of estimate was 0.087. Conclusion The DATT can be used to monitor for changes in peritoneal transport over time. It should not be used in patients receiving cycler therapy or in patients whose dwell times and dextrose concentrations vary markedly from day to day.
STING manifests self DNA-dependent inflammatory disease

Inflammatory autoimmune diseases such as systemic lupus erythematosus (SLE) and polyarthritis are characterized by chronic cytokine overproduction, suggesting that the stimulation of host innate immune responses, speculatively by persistent infection or self nucleic acids, plays a role in the manifestation of these disorders. Mice lacking DNase II die during embryonic development through comparable inflammatory disease because phagocytosed DNA from apoptotic cells cannot be adequately digested and intracellular host DNA sensor pathways are engaged, resulting in the production of a variety of cytokines including type I IFN. The cellular sensor pathway(s) responsible for triggering DNA-mediated inflammation aggravated autoimmune disease remains to be determined. However, we report here that Stimulator of IFN Genes (STING) is responsible for inflammation-related embryonic death in DNase II defective mice initiated by self DNA. DNase II-dependent embryonic lethality was rescued by loss of STING function, and polyarthritis completely prevented because cytosolic DNA failed to robustly trigger cytokine production through STING-controlled signaling pathways. Our data provides significant molecular insight into the causes of DNA-mediated inflammatory disorders and affords a target that could plausibly be therapeutically controlled to help prevent such diseases.
Structural alterations of airway epithelial tight junctions in cystic fibrosis: comparison of transplant and postmortem tissue.

Previous descriptive freeze-fracture studies have suggested that the airway epithelium in cystic fibrosis (CF) is associated with proliferation and basal extension of tight junctional elements. The significance of these reports in CF has been difficult to evaluate because tight junctions are labile structures, capable of alteration, postmortem. The aim of the present study was to test the hypothesis that the abnormalities in tight junction structure reported previously are unique to CF airways, and to determine the confounding effects of postmortem autolysis. To this end, we analyzed human airway epithelial tight junctions in: (1) histologically normal tissue taken from lungs resected for pulmonary tumor (i.e., resection controls), (2) lungs from patients who died of nonrespiratory causes (i.e., postmortem controls), (3) lungs removed from CF patients undergoing transplantation, and (4) lungs from CF patients postmortem. Tight-junctional depth, strand number, and junctional complexity were analyzed. Basal extensions and isolated foci of tight-junctional elements were found in all groups except for the resection controls. The following two parameters were therefore assessed: (1) the number of times a junction extended below the maximal depth found in the resection controls and (2) the extent of junctional elements that were isolated and distant from the apico-lateral junctional belt. The mean frequencies of occurrence of junctional extension beyond the normal maximum were 4.8% for the CF transplant, 23.6% for the control postmortem, and 48.8% for the CF postmortem group. (ABSTRACT TRUNCATED AT 250 WORDS)
Confabulations in Episodic Memory Are Associated With Delusions in Alzheimer’s Disease

Although confabulations and delusions are observed in Alzheimer’s disease, the relationship between the 2 has not been fully investigated. This study involved 50 patients with Alzheimer’s disease and 10 healthy participants. After the patients were divided into delusional and nondelusional groups, confabulations and cognitive function were assessed. No confabulations appeared in the healthy participants, and only patients with Alzheimer’s disease showed confabulations. The delusional group produced more confabulations on episodic subjects than on semantic subjects. There was a correlation between cognitive impairment and confabulations in semantic memory. These findings suggest that different mechanisms are involved in confabulations between semantic and episodic memories.
Specification-driven validation of programmable embedded systems

Validation of programmable embedded systems, consisting of processor cores, coprocessors, and memory subsystems, is one of the major bottleneck in current System-on-Chip (SOC) design methodology. One of the most important problems in validation of such systems is the lack of a golden reference model. As a result, many existing validation techniques employ a bottom-up approach to design verification, where the functionality of an existing architecture is, in essence, reverse-engineered from its implementation. This thesis presents a top-down validation methodology that complements the existing bottom-up approaches. It leverages the system architect's knowledge about the behavior of the design through architecture specification. We have developed validation techniques to ensure that the static and dynamic behaviors of the specified architecture is well formed. The validated specification is used as a golden reference model. A major challenge in top-down validation methodology is the ability to generate executable models from the specification for a wide variety of programmable architectures. We have developed a functional simulation, hardware generation, and property checking. The generated simulator and hardware models are used for design space exploration of programmable architectures. We have explored two top-down validation scenarios: design validation and test generation. First, the generated hardware is used as a reference model to verify the hand-written implementation using a combination of symbolic simulation and equivalence checking. Second, we have proposed a functional coverage based test generation technique for validation of pipelined processor architectures. The experiments demonstrate the utility of the specification-driven validation methodology for programmable embedded systems.
Induction of Supernova-like Explosions by Gamma-Ray Bursts in Close Binary Systems

We propose that a gamma-ray burst in one member of a binary may induce a supernova-like explosion of a close, white dwarf companion. Such an explosion might be brought about in rather light companions, which cannot undergo the standard accretion-induced explosion. This would give some supernovae associated with gamma-ray bursts an appearance rather unlike that of the typical Type I supernova. GRB 980425, if indeed associated with SN 1998bw, is too weak to have produced the latter through our proposed mechanism.
Use of intracellular Ca2+ stores from rat basophilic leukemia cells to study the molecular mechanism leading to quantal Ca2+ release by inositol 1,4,5-trisphosphate.

Quantal Ca2+ release is a novel motif for the mediation of signal transduction in which the amplitude of a biological response following multiple stepwise increases in agonist concentration is retained. The release of Ca2+ from permeabilized cells in response to the second messenger inositol 1,4,5-trisphosphate (InsP3) proceeds in this fashion. The mechanisms leading to quantal Ca2+ release are unknown. InsP3 releases 50-90% of the Ca2+ sequestered within the intracellular stores of mammalian cells permeabilized with saponin. However, preparation of microsomes results in the loss of this sensitivity. In this report, functionally intact intracellular Ca2+ stores were isolated from rat basophilic leukemia (RBL) cells by osmotic lysis followed by differential and sucrose density gradient centrifugation. From this preparation, 64% of the stored Ca2+ is released by InsP3. We demonstrate that quantal Ca2+ release is retained by isolated Ca2+ stores and is identical to that observed in permeabilized cells. Addition of a subsaturating (28 nM) concentration of InsP3 to permeabilized cells at 37 degrees C results in the release of only a small fraction of the sequestered Ca2+. When the cells are cooled to 11 degrees C, the remaining Ca2+ is rapidly released. Hence, the mechanism leading to the quantal nature of Ca2+ release is reversible and is thus not likely to be the result of a covalent modification of the channel protein or of the Ca2+ store. (ABSTRACT TRUNCATED AT 250 WORDS)
Regioselective acylation of disaccharides in tert‐butyl alcohol catalyzed by Candida antarctica lipase

The acylation of several disaccharides by ethyl butanoate and ethyl dodecanoate was catalyzed by Candida antarctica lipase in tert‐butyl alcohol, at temperatures ranging from 40° to 82°C (reflux temperature). The relative reaction rates of the various disaccharides were directly related to their solubility. The primary products were the monoesters derived from acylation of the primary alcohol groups. At higher conversions diesters were formed, and the ratio of diester to monoester was markedly dependent on the structure of the disaccharide. Thus, reaction of maltose with ethyl dodecanoate in refluxing tert‐butyl alcohol afforded the 6′‐monododecanoate even at high conversions. Trehalose, in contrast, afforded the 6,6′‐diester. Acylation of the less soluble sucrose and lactose was much slower, but a moderate (37%) conversion of sucrose was observed after a prolonged reaction time (7 days). A number of other lipases and proteases were tested but C. antarctica lipase was unique in catalyzing the acylation of sucrose in refluxing tert‐butyl alcohol. © 1996 John Wiley & Sons, Inc.
Organization of flexor–extensor interactions in the mammalian spinal cord: insights from computational modelling

Alternation of flexor and extensor activity in the mammalian spinal cord is mediated by two classes of genetically identified inhibitory interneurons, V1 and V2b. The V1 interneurons are essential for high‐speed locomotor activity. They secure flexor–extensor alternations in the intact cord but lose this function after hemisection, suggesting that they are activated by inputs from the contralateral side of the cord. The V2b interneurons are involved in flexor–extensor alternations in both intact cord and hemicords. We used a computational model of the spinal network, simulating the left and right rhythm‐generating circuits interacting via several commissural pathways, and extended this model by incorporating V1 and V2b neuron populations involved in flexor–extensor interactions on each cord side. The model reproduces multiple experimental data on selective silencing and activation of V1 and/or V2b neurons and proposes the organization of their connectivity providing flexor–extensor alternation in the spinal cord.
Therapeutic efficacy and tolerability of brodimoprim in comparison with doxycycline in acute sinusitis in adults.

OBJECTIVE To compare efficacy and tolerability of brodimoprim tablets with doxycycline tablets in adults with acute sinusitis. DESIGN Open, randomized, controlled phase III study, with parallel groups. PATIENTS Of the 70 enrolled patients, 56 adults of both sexes with a mean age of 33 years were evaluable. STUDY DRUGS: One brodimoprim 200mg tablet or one doxycycline 100mg tablet was administered once daily for 8 to 12 days (on the first treatment day all patients received the loading dose consisting of 2 tablets of the corresponding compound). CLINICAL OUTCOME In the brodimoprim group 96.4% of the patients were judged cured/improved; in the doxycycline group 96.2%. BACTERIOLOGICAL OUTCOME: Eradication of the causative pathogen/s was achieved in 87.5% of the patients treated with brodimoprim and in 60% of the doxycycline group. SAFETY OUTCOME: Tolerability was judged as very good/good in 89.7% of the patients treated with brodimoprim and in all patients receiving doxycycline. Gastrointestinal skin, CNS and various other reactions were reported by 13 patients; 3 of them had to discontinue treatment. Discontinuation of therapy: 8 more patients withdrew from the study due to inactivity of the compound or reasons unrelated to the drugs. CONCLUSION Brodimoprim was shown to be effective in the treatment of acute sinusitis in adults, its efficacy being equal to that of doxycycline. The assessments showed a positive clinical response to the medication in 96.4% of the patients treated with brodimoprim and 96.2% of the patients taking doxycycline. Both compounds were well tolerated and all side effects were of mild nature and reversible.
Linking the antigen archive structure to pathogen fitness in African trypanosomes

Systems that generate antigenic variation enable pathogens to evade host immune responses and are intricately interwoven with major pathogen traits, such as host choice, growth, virulence and transmission. Although much is understood about antigen switching at the molecular level, little is known about the cross-scale links between these molecular processes and the larger-scale within and between host population dynamics that they must ultimately drive. Inspired by the antigenic variation system of African trypanosomes, we apply modelling approaches to our expanding understanding of the organization and expression of antigen repertoires, and explore links across these scales. We predict how pathogen population processes are determined by underlying molecular genetics and infer resulting selective pressures on important emergent repertoire traits.