Miracle-dz/UniFAR-FTUs huggingface dataset:
Lasso and equivalent quadratic penalized models

The least absolute shrinkage and selection operator (lasso) and ridge regression produce usually different estimates although input, loss function and parameterization of the penalty are identical. In this paper we look for ridge and lasso models with identical solution set. It turns out, that the lasso model with shrink vector $\lambda$ and a quadratic penalized model with shrink matrix as outer product of $\lambda$ with itself are equivalent, in the sense that they have equal solutions. To achieve this, we have to restrict the estimates to be positive. This doesn't limit the area of application since we can easily decompose every estimate in a positive and negative part. The resulting problem can be solved with a non negative least square algorithm. Beside this quadratic penalized model, an augmented regression model with positive bounded estimates is developed which is also equivalent to the lasso model, but is probably faster to solve.
Bologna Translation Service: Online translation of course syllabi and study programmes in English

BTS – Bologna Translation Service – is an ICT PSP EU-funded project which specializes in the automatic translation of study programmes. At the core of the BTS framework are several machine translation (MT) engines through which web-based translation services are offered. The fully integrated BTS architecture includes a translation engine coupling rule-based and statistical MT with automatic post-editing (APE). In this paper, we first describe the motivating factors behind the provision of such a service. Following this, we give an overview of the BTS framework as a whole, with particular emphasis on the MT components, and provide a real world use case scenario in which BTS MT services are exploited.
Can the built environment explain gender gap in cycling? An exploration of university students' travel behavior in Toronto, Canada

ABSTRACT The benefits of cycling as a healthier and more sustainable transportation alternative to private automobile is emphasized in both literature and policy. One key policy challenge in improving cycling rates is the significant gender gap in cycling that exists across urban regions in North America. In this study, travel behavior of >10,000 students attending four universities in Toronto, Canada, was analyzed to explore gender-based differences in cycling uptake. The mode share for cycling was higher for non-commute trips (9%) when compared to commuting trips to universities (7.6%). In addition, men had higher cycling rates than women, for both commute and non-commute trips. Results from binomial logistic regression models indicate that the built environment-related correlates were different between male and female students, and between commute and non-commute trips. Access to bicycle lanes or cycle tracks was found to increase the odds of female commuter cycling. This effect, however, was moderate in the neighborhoods with higher land use mix. Further, high-speed traffic was a significant barrier to cycling among female commuters. Noticeably, our analysis did not find major gender-based differences in the coefficients relating to travel attitudes and preferences. The findings provide a Canadian comparison to the limited international research on this topic, as well as offer new insights particularly relating to cycling for non-commute trips. The results identify potential avenues for policy intervention regarding the promotion of healthy and sustainable travel behavior among post-secondary students, and more broadly, the millennial generation.
Identification of Regions Required for Apical Membrane Localization of Human Multidrug Resistance Protein 2

Multidrug resistance proteins MRP1 and MRP2 transport a wide range of endo- and xenobiotics. However, with the exception of certain parts of the brain, MRP1 traffics to basolateral membranes of polarized cells, whereas MRP2 is apical in location and thus it is particularly important for systemic elimination of such compounds. Different regions of MRP1 and MRP2 seem to target them to their respective membrane locations. In addition to two “core” membrane spanning domains (MSDs) characteristic of ATP-binding cassette transporters, MRP1 and MRP2 have a third NH2-terminal MSD (MSD0), which is not required for basolateral targeting of MRP1, or for transport of at least some substrates. Here, we demonstrate that all elements necessary for apical targeting of MRP2 reside in MSD0 and the adjacent cytoplasmic loop (CL) 3. Furthermore, we show that this region of MRP2 can target the core of MRP1 to an exclusively apical location. Within MRP2 CL3, we identified a lysine-rich element that is essential for apical targeting. When introduced into MRP1, this element alone is sufficient to result in partial apical localization. However, exclusive targeting to the apical membrane seems to require the integrity of the entire region encompassing MSD0 and CL3 of MRP2. Because CL3 of MRP1 is critical for binding, transport, or both of several compounds, we also examined the function of hybrids containing all, or portions of MRP2 MSD0 and CL3. Our results indicate that CL3 is important for interaction with both the glutathione and glucuronide conjugates tested, but that different regions may be involved.
Enamel Defects and Ameloblast-specific Expression in Enam Knock-out/lacZ Knock-in Mice*

Enamelin is critical for proper dental enamel formation, and defects in the human enamelin gene cause autosomal dominant amelogenesis imperfecta. We used gene targeting to generate a knock-in mouse carrying a null allele of enamelin (Enam) that has a lacZ reporter gene replacing the Enam translation initiation site and gene sequences through exon 7. Correct targeting of the transgene was confirmed by Southern blotting and PCR analyses. No enamelin protein could be detected by Western blotting in the Enam-null mice. Histochemical 5-bromo-4-chloro-3-indolyl-β-d-galactopyranoside (X-gal) staining demonstrated ameloblast-specific expression of enamelin. The enamel of the Enam+/- mice was nearly normal in the maxillary incisors, but the mandibular incisors were discolored and tended to wear rapidly where they contacted the maxillary incisors. The Enam-/- mice showed no true enamel. Radiography, microcomputed tomography, and light and scanning electron microscopy were used to document changes in the enamel of Enam-/- mice but did not discern any perturbations of bone, dentin, or any other tissue besides the enamel layer. Although a thick layer of enamel proteins covered normal-appearing dentin of unerupted teeth, von Kossa staining revealed almost a complete absence of mineral formation in this protein layer. However, a thin, highly irregular, mineralized crust covered the dentin on erupted teeth, apparently arising from the formation and fusion of small mineralization foci (calcospherites) in the deeper part of the accumulated enamel protein layer. These results demonstrate ameloblast-specific expression of enamelin and reveal that enamelin is essential for proper enamel matrix organization and mineralization.
Obesity is a common comorbidity for pediatric patients with untreated, newly diagnosed epilepsy

Objective: This study aimed to determine the frequency and factors associated with obesity in a cohort of children and adolescents with newly diagnosed untreated epilepsy. Methods: Body mass index (BMI) Z-scores and percentiles, both adjusted for age, were used as measures for obesity. Potential covariates associated with these BMI measures included age, etiology (cryptogenic, idiopathic, symptomatic), seizure type (generalized, partial, unclear), concomitant medications (stimulants, nonstimulants, none), and insurance status (privately insured, Medicaid). The primary analysis compared the epilepsy patients’ BMI Z-scores to Centers for Disease Control and Prevention data for healthy children. The secondary analysis compared the epilepsy patients’ BMI Z-scores to those of a regional healthy control group. Additional analyses incorporated the secondary outcome measure BMI percentiles indexed for age. Results: Children with newly diagnosed untreated epilepsy had higher BMI Z-scores compared to standard CDC growth charts (p < 0.0001) and the healthy control cohort (p = 0.0002) specifically at both of the 2 tail ends of the distribution. Overall, 38.6% of the epilepsy cohort were overweight or obese (BMI ≥85th percentile for age). Differences in age, etiology, and concomitant nonepilepsy medications were significantly associated with variability in age-adjusted BMI Z-score. Patients in adolescence had higher adjusted BMI Z-scores than younger patients. Patients with symptomatic epilepsy had lower adjusted BMI Z-scores than patients with idiopathic epilepsy. Patients on stimulant psychotropics exhibited lower adjusted BMI Z-scores than patients on no medication. Conclusion: Obesity is a common comorbidity in children with newly diagnosed untreated epilepsy and correlates with increasing age, idiopathic etiology, and absence of concomitant medication.
Direct olfactory transport of inhaled manganese ((54)MnCl(2)) to the rat brain: toxicokinetic investigations in a unilateral nasal occlusion model.

Inhalation exposure of humans to high concentrations of manganese (Mn) is associated with elevated Mn levels in the basal ganglia and an extrapyramidal movement disorder. In the rat, direct olfactory transport of Mn from the nose to the brain has been demonstrated following intranasal instillation of (54)MnCl(2). However, the contribution this route makes to brain Mn delivery following inhalation is unknown and was the subject of our study. Male 8-week old CD rats underwent a single 90-min nose-only exposure to a (54)MnCl(2) aerosol (0.54 mg Mn/m(3); MMAD 2.51 microm). The left and right sides of the nose and brain, including the olfactory pathway and striatum, were sampled at 0, 1, 2, 4, and 8 days postexposure. Control rats were exposed to (54)MnCl(2) with both nostrils patent to evaluate the symmetry of Mn delivery. Another group of rats had the right nostril plugged to prevent nasal deposition of (54)MnCl(2) on the occluded side. Gamma spectrometry (n = 6 rats/group/time point) and autoradiography (n = 1 rat/group/time point) were used to compare the levels of (54)Mn found on the left and right sides of the nose and brain to determine the contribution of olfactory uptake to brain (54)Mn levels. Brain and nose samples from the side with the occluded nostril had negligible levels of (54)Mn activity, validating the nasal occlusion procedure. High levels of (54)Mn were observed in the olfactory bulb and tract/tubercle on the side or sides with an open nostril within 1-2 days following inhalation exposure. These results demonstrated, for the first time, that the olfactory route contributes the majority (up to >90%) of the (54)Mn found in the olfactory pathway, but not in the striatum, of the rat brain up to 8 days following a single inhalation exposure. These findings suggest that the olfactory route may make a significant contribution to brain Mn levels following inhalation exposure in the rat.
Ectopic expression of c‐jun leads to differentiation of P19 embryonal carcinoma cells.

The product of the c‐jun proto‐oncogene, a major component of the transcription factor AP1, has been implicated in both positive and negative transcriptional control as well as in transformation. The role of c‐jun in early development and differentiation processes, however, is still largely unknown. In this paper we show that ectopic expression of exogenous c‐jun sequences leads to differentiation and loss of the transformed phenotype of P19 embryonal carcinoma (EC) cells. The mixed populations of endoderm‐ and mesoderm‐like cells that were obtained after the introduction of c‐jun morphologically and biochemically resembled P19 cells differentiated in monolayer by retinoic acid (RA). Furthermore, we provide evidence that direct effects of the c‐jun gene product on transcription of the retinoic acid receptor beta (RAR beta) gene may be responsible for the differentiation‐promoting potential of c‐jun.
Relationships between peak torque, peak angular impulse, and average power in the thigh muscles of subjects with knee damage.

The purpose of this study was to determine the relationship between the isometric and isokinetic peak torque (PT) (speed of movement 0, 60, and 180 deg/s) and the peak angular impulse (PAI) and average power (AP) of multiple contractions (180 deg/s) of the quadriceps and hamstrings in 29 patients with a chronic, complete deficiency of the medial collateral ligament (MCL) of the knee. At every test speed the Pearson product moment (r) and the Spearman rank (rs) correlation coefficients between the PT and PAI were highly significant for both muscle groups in the uninjured (r = .81-.97, rs = .77-.97) as well as in the MCL deficient (r = .77-.97, rs = .75-.95 knees. The results were the same between the PT and AP (uninjured knee: r = .83-.98, rs = .82-.98; MCL deficient knee: r = .78-.97, rs = .76-.97). In both knees and in both muscle groups the correlation coefficients increased toward the highest speed of the isokinetic movement, obviously because the PAI and AP were registered at that speed. In conclusion, concerning MCL deficient or uninjured knees the PAI or AP analysis may offer little additional information about thigh muscle function to that attained by more simple measurement, the PT analysis.
Comparing Abstract Numerical and Visual Depictions of Risk in Survey of Parental Assessment of Risk in Sickle Cell Hydroxyurea Treatment

Communicating risk is an important activity in medical decision-making; yet, numeracy is not a universal skill among the American public. We examined the hypothesis that numerical risk information about the use of hydroxyurea for children with sickle cell disease would elicit different risk assessment responses when visual depictions were used instead of abstract numbers and depending on the disease severity. Parents of 81 children with sickle cell disease participated in a survey in which hydroxyurea was first described as carrying a certain chance of risk for both birth defects and cancer. Then, the parents indicated the highest risk at which they would hypothetically consent to the treatment to help their child. Risk presentations were repeated with abstract numerical, pie graph, and 1000 people histogram formats. The &khgr;2 analyses comparing high-risk to low-risk assessment across presentation formats showed high consistency between visual depictions but low consistency of abstract numerical with visual depictions. The parents of children with SC and other less severe types of SCD were less willing to accept higher risk than those with SS when the data were presented numerically. Given earlier concerns about poor “numeracy” in the US population, visual depictions of risk could be an effective tool for routine communication in health education and medical decision-making.
SERUM PROLACTIN AND THE SUPPRESSION OF LACTATION

Baromocriptine (2 bromo‐α‐ergocryptine), stilboestrol, clomiphene citrate, testosterone propionate and a placebo were given to 75 postpartum women for the suppression of puerperal lactation. An additional 15 women who breast‐fed their babies served as a control group. Blood samples were taken for the determination of serum prolactin levels by a specific homologous double antibody radioimmuno‐assay. Concurrently, the clinical effectiveness of the various treatments was assessed. High levels of prolactin were found at the time of delivery. Bromocriptine effectively reduced serum prolactin and prevented lactation; stilboestrol increased serum prolactin and partially suppressed lactation; clomiphene citrate and testosterone propionate both lowered serum prolactin levels and partially suppressed lactation. The placebo showed almost no effect on serum prolactin. It appeared that bromocriptine was the drug of choice in the suppression of puerperal lactation.
Relative merits of immunohistochemical demonstrations of placental, A, B and C forms of glutathione S-transferase and histochemical demonstration of gamma-glutamyl transferase as markers of altered foci during liver carcinogenesis in rats.

The values of the immunohistochemical demonstrations of glutathione S-transferases (GSTs) A, B, C and P and histochemical demonstrations of gamma-glutamyl transpeptidase (gamma-GT) for detection of enzyme altered foci in F344 rat liver were compared. Rats were given a single i.p. injection of 200 mg/kg body weight of diethylnitrosamine (DENA), from 2 weeks later they were given 0.02% N-2-fluorenylacetamide (2-FAA), phenobarbital (PB), butylated hydroxyanisole (BHA) or butylated hydroxytoluene (BHT) in their diet for 6 weeks and then they were given basal diet and tap water for 4 weeks. They were subjected to partial hepatectomy at the end of week 3. Results showed that immunohistochemical demonstration of GSTs A, B and C for detection of foci were only effective when the administration of 2-FAA, PB, BHA or BHT in the diet was discontinued, because these GSTs were induced in surrounding hepatocytes by these compounds in the diet. gamma-GT was induced in periportal hepatocytes strongly by BHA and BHT and slightly by PB, and gamma-GT positive foci in periportal areas were not distinguishable from gamma-GT positive periportal hepatocytes. GST-P was also induced moderately by BHA and slightly by BHT in periportal hepatocytes, but all GST-P positive foci were clearly distinguishable. In addition, almost all gamma-GT positive foci gave a positive reaction for GST-P, but 5-10% of the GST-P positive foci were not gamma-GT positive.
Novel role of FATP1 in mitochondrial fatty acid oxidation in skeletal muscle cells

Carnitine palmitoyltransferase 1 (CPT1) catalyzes the first step in long-chain fatty acid import into mitochondria, and it is believed to be rate limiting for &bgr;-oxidation of fatty acids. However, in muscle, other proteins may collaborate with CPT1. Fatty acid translocase/CD36 (FAT/CD36) may interact with CPT1 and contribute to fatty acid import into mitochondria in muscle. Here, we demonstrate that another membrane-bound fatty acid binding protein, fatty acid transport protein 1 (FATP1), collaborates with CPT1 for fatty acid import into mitochondria. Overexpression of FATP1 using adenovirus in L6E9 myotubes increased both fatty acid oxidation and palmitate esterification into triacylglycerides. Moreover, immunocytochemistry assays in transfected L6E9 myotubes showed that FATP1 was present in mitochondria and coimmunoprecipitated with CPT1 in L6E9 myotubes and rat skeletal muscle in vivo. The cooverexpression of FATP1 and CPT1 also enhanced mitochondrial fatty acid oxidation, similar to the cooverexpression of FAT/CD36 and CPT1. However, etomoxir, an irreversible inhibitor of CPT1, blocked all these effects. These data reveal that FATP1, like FAT/CD36, is associated with mitochondria and has a role in mitochondrial oxidation of fatty acids.
Functional characterization of the PP2C phosphatase CaPtc2p in the human fungal pathogen Candida albicans

Type 2C protein phosphatases (PP2C) are monomeric enzymes and their activities require the presence of magnesium or manganese ion. There are seven PP2C‐like genes in Candida albicans. In this study, we demonstrate that CaPtc2p is a PP2C phosphatase. Surprisingly, in addition to the cytoplasmic localization, CaPtc2p is partially associated with mitochondria in yeast‐form and filamentous cells of C. albicans. Expression of CaPTC2 is developmentally regulated during the serum‐induced filamentation. Deletion of CaPTC2 renders C. albicans cells sensitive to SDS and azole antifungals, as well as the DNA methylation agent methylmethane sulphonate and the DNA synthesis inhibitor hydroxyurea. Therefore, CaPtc2p might fulfil multiple functions, including the regulation of mitochondrial physiology and checkpoint recovery from DNA damage in C. albicans cells. Copyright © 2010 John Wiley & Sons, Ltd.
Anatomical and Histological Changes in the Alimentary Tract of Migrating Blackcaps (Sylvia atricapilla): A Comparison among Fed, Fasted, Food‐Restricted, and Refed Birds

During northward migration, blackcaps that arrive to refuel at stopover sites in Israel’s Negev Desert have reduced masses of organs that are important in food digestion and assimilation. We tested several predictions from the general hypothesis that smaller organs of digestion (small intestine and pancreas) and nutrient assimilation (liver) bring about a lower capacity to consume food and that the organs must be restored before blackcaps can feed and digest at a high rate. We used a fasting protocol to create a group of blackcaps with reduced intestine and liver mass (reduced by 45% and 36%, respectively) compared with controls fed ad lib. Because most of the small intestine’s biochemical digestive capacity reside in enterocytes found on villi, we predicted and found that reduced intestinal mass in fasted blackcaps related mainly to changes in enterocytes rather than other cells and tissues such as nonabsorptive crypt cells or underlying muscle. Because migrating blackcaps that stop over to feed begin to increase in body mass only 2 d after arrival, we predicted and found a similar recovery period in blackcaps that were first fasted but then refed—the organ mass, structure, function, and ability to consume food was restored after 2 d of feeding. Another group of food‐restricted blackcaps (fed at one‐third ad lib. level) lost similar amounts of body mass as fasted blackcaps but had much greater capacity to consume food than fasted blackcaps, and so we predicted that they would exhibit little or no reduction in alimentary organs relative to controls fed ad lib. A surprising result was that, as in fasted blackcaps, in food‐restricted blackcaps, the decreases in masses of small intestine, liver, and pancreas were proportionally greater than the decreases in body mass or in masses of nonalimentary organs (heart, pectoralis). Food restriction, like fasting, caused a decrease in amount of intestinal mucosa and an alteration in the phenotype of enterocytes. These results are thus not consistent with the general hypothesis, and although they can be rationalized by assuming that blackcaps fed ad lib. have excess digestive capacity, it may also be that the physiological process or processes limiting very high feeding rate lie elsewhere than in the digestive system.
Increased Expression of NGFI‐A mRNA in the Rat Striatum Following Burst Stimulation of the Medial Forebrain Bundle

Using in situ hybridization, we examined the mRNA expression for several immediate early genes in dopamine‐innervated brain areas following electrical burst vs. regular stimulation of the medial forebrain bundle in anaesthetized rats. Two hours after 5 Hz burst stimulation, the expression of the nerve growth factor‐inducible clone A (NGFI‐A) mRNA was increased in the medial part of the striatum. This increase was prevented by pretreatment with the dopamine‐D1 receptor antagonist, SCH23390 (0.1 mg/kg i.p.). After 8 Hz burst stimulation, NGFI‐A mRNA expression was increased in the medial, central and lateral parts of the striatum. Induction occurred predominantly in cells expressing mRNAs for the dopamine‐D1 receptor, substance P and dopamine and CAMP‐regulated phosphoprotein (DARP‐32). Regular stimulation had no effect on NGFI‐A mRNA expression. The induction of NGFI‐A was related to the levels of dopamine released by burst or regular stimulation as demonstrated with in vivo amperometry. Two hours after stimulation, the expression of none of the other genes studied was altered. One hour after 8 Hz burst stimulation, the expression of NGFI‐A, NGFI‐B and jun‐B mRNAs was increased in the striatum and that of NGFI‐A, NGFI‐6, c‐fos, fos‐B and jun‐B mRNAs was variably increased in the nucleus accumbens and lateral septum. These results provide additional support for the physiological importance of burst firing activity in midbrain dopamine neurons for the activation of their target cells. They demonstrate a spatial and temporal specificity as regards the brain region, the gene activated, the receptor involved and the phenotype of the cells affected.