Miracle-dz/UniFAR-FTUs huggingface dataset:
Physiological response of high-level female judokas measured through laboratory and field tests. Retesting the validity of the Santos test.

AIM The aim of the study was to measure the physiological demands of a group of high-level female judokas through laboratory tests and field tests (Tatami) and to retest the validity of the Santos test on a different population. METHODS Eight high-level female judokas participated in the study. Heart rate (HR), maximal oxygen consumption (VO2 max), blood lactate, anaerobic threshold, and ratings of perceived exertion (RPE) were measured using laboratory and field tests that shared common characteristics. RESULTS The mean (±SD) values obtained in the laboratory tests were HRmax 198.3 (4.1) beats.min-1, VO2 max: 40.9 (7.7) mL.kg-1.min-1, lactate max 9.1 (1.4) mmol.L-1, HR at the anaerobic threshold 171.5 (4.8) beats.min-1, lactate threshold 3.8 (0.4) mmol.L-1, and RPE: 17 (1.1). The mean (±SD) values obtained in the field test were HRmax 199.0 (5.0) beats.min-1, VO2 max: 44.8 (7.3) mL.kg-1.min-1, lactate max: 11.8 (1.5) mmol.l-1, HR at the anaerobic threshold 170.5 (3.2) beats.min-1, lactate threshold: 3.8 (0.1) mmol.L-1, and RPE: 18 (1.4) points. There were no significant differences between the data obtained on both tests in any of the parameters, except for the lactate maximum and VO2 max. CONCLUSION The Santos test is a helpful instrument for judo training in female athletes. Coaches could use it to design specific training protocols that could help to improve their performance in competition.
The Critical Role of LIGHT, a TNF Family Member, in T Cell Development1

Negative selection refers to the selective deletion of autoreactive thymocytes but its molecular events have not been well defined. In this study, we demonstrate that a cellular ligand for herpes virus entry mediator and lymphotoxin receptor (LIGHT), a newly identified member of the TNF superfamily, may play a critical role in negative selection. Using TCR transgenic mice, we find that the blockade of LIGHT signaling in vitro and in vivo prevents negative selection induced by peptide and intrathymically expressed Ags, resulting in the rescue of thymocytes from apoptosis. Furthermore, the thymi of LIGHT transgenic mice show severe atrophy with remarkably reduced CD4+CD8+ double-positive cells caused by increased apoptosis, suggesting that LIGHT can delete immature T cells in vivo. Taken together, these results demonstrate a critical role of LIGHT in thymic negative selection of the T cell repertoire.
Attentional functioning and white matter integrity among survivors of malignant brain tumors of childhood

Children surviving treatment for malignant brain tumors commonly have problems maintaining their premorbid levels of intellectual development and academic achievement. Our group has been especially interested in the effects of treatment on normal appearing white matter (NAWM) on MRI and the influence of NAWM volumes on neurocognitive functioning. The present study assessed NAWM and attentional abilities among 37 long-term survivors of malignant brain tumors, ranging in age from 1.7 to 14.8 (Mdn = 6.5) years at diagnosis, who had been treated with cranial radiation therapy with or without chemotherapy 2.6 to 15.3 (Mdn = 5.7) years earlier. On the Conners' Continuous Performance Test, the Overall Index and 7 of the other 10 indices were significantly deficient compared to age- and gender-corrected normative values. After statistically controlling for the effects of age at diagnosis and time elapsed from treatment, 5 of the 8 indices were significantly associated with cerebral white matter volumes and/or specific regional white matter volumes of the prefrontal/frontal lobe and cingulate gyrus. No gender effects were observed. The results of the present study further support the contention that NAWM is an important substrate for treatment-induced neurocognitive problems among survivors of malignant brain tumors of childhood. (JINS, 2004, 10, 180–189.)
Brain potentials to native phoneme discrimination reveal the origin of individual differences in learning the sounds of a second language

Human beings differ in their ability to master the sounds of their second language (L2). Phonetic training studies have proposed that differences in phonetic learning stem from differences in psychoacoustic abilities rather than speech-specific capabilities. We aimed at finding the origin of individual differences in L2 phonetic acquisition in natural learning contexts. We consider two alternative explanations: a general psychoacoustic origin vs. a speech-specific one. For this purpose, event-related potentials (ERPs) were recorded from two groups of early, proficient Spanish-Catalan bilinguals who differed in their mastery of the Catalan (L2) phonetic contrast /e-ε/. Brain activity in response to acoustic change detection was recorded in three different conditions involving tones of different length (duration condition), frequency (frequency condition), and presentation order (pattern condition). In addition, neural correlates of speech change detection were also assessed for both native (/o/-/e/) and nonnative (/o/-/ö/) phonetic contrasts (speech condition). Participants' discrimination accuracy, reflected electrically as a mismatch negativity (MMN), was similar between the two groups of participants in the three acoustic conditions. Conversely, the MMN was reduced in poor perceivers (PP) when they were presented with speech sounds. Therefore, our results support a speech-specific origin of individual variability in L2 phonetic mastery.
Neuropsychological Markers of Progression From Mild Cognitive Impairment to Alzheimer’s Disease

To find early clinical markers that may predict a likely progression to Alzheimer’s disease (AD), the authors performed neuropsychological tests on 82 mild cognitive impairment (MCI) subjects. After 3 years, 38 patients developed AD while 44 retained the diagnosis of MCI. The cognitive differences between the groups were studied. Patients who developed AD showed significantly lower values than did MCI subjects in some neuropsychological scores (P = .02-.001), with sensitivities and specificities higher than 84% and 64%, respectively, for detecting early-onset AD, with a 7.9-fold increased risk of converting to AD (P < .001). Regarding the logistic regression model, the CAMCOG Memory and Perception cognitive screening items were the optimum independent tools to classify the patients who will progress to AD, showing a relative risk of progression of 10.5 (P = .002), 5.5 (P = .008), and 3.9 times (P = .05), respectively, with a sensibility of of 92.1% and a specificity 72.7%.
Neuroarchitecture of the central complex in the brain of the locust Schistocerca gregaria and S. americana as revealed by serotonin immunocytochemistry

The central complex is a prominent structure in the insect brain, yet its anatomical organization and functional role is still poorly understood. To facilitate investigations on the physiology of the central complex, this study describes its anatomical organization in the brain of locusts (Schistocerca gregaria and Schistocerca americana) based on an investigation of serotonin immunocytochemistry. Most subdivisions of the central complex including the protocerebral bridge, several layers in the upper division of the central body, and the noduli of the central body are innervated by serotonin‐immunoreactive neurons, while the lower division of the central body does not exhibit serotonin‐like immunoreactivity. Several types of serotonin‐immunoreactive neurons can be distinguished. A system of about 60 columnar neurons innervates the protocerebral bridge, layer III of the upper division of the central body, and the noduli. A group of 15–20 bilateral pairs of serotonin‐immunoreactive neurons connects the posterior optic tubercles with the protocerebral bridge. About ten pairs of neurons with somata in the inferior protocerebrum innervate layer la of the upper division of the central body. In addition, large‐field neurons arborize in layers Ia and Ib of the upper division of the central body and in the lateral accessory lobes. The detailed mapping of serotonin immunoreactivity provides further insight into the anatomical organization of the central complex and suggests that serotonin is a major neuroactive substance within this brain structure.
Antigenic variation in Giardia lamblia: cellular and humoral immune response in a mouse model

Summary Neonatal mice (CR:NIH:S) were infected with a cloned human isolate of Giardia lamblia (GS/M‐83‐H7) and the surface antigens of the intestinal trophozoites, as well as the cellular and humoral immune responses, were analysed during the course of infection. Infections in mice peaked 2–3 weeks after inoculation and were self‐cured by day 42 post‐infection (p.i.). The proportion of trophozoites expressing the Mr 72 000 surface antigen of the initial inoculum had decreased by day 12 and approached zero by day 22 p.i. , similar to infections in humans. The predominant parasite‐specific humoral response was an IgM‐ and IgG‐isotype directed to the original Mr 72 000 surface antigen as well as other antigens. T‐lymphocytes (predominantly LY4(CD4)+) isolated from Peyer's patches 12 days p.i. and later showed a significant proliferative response to Giardia lamblia antigens. Spleen and lymph node cells showed no lymphoproliferative response. T‐cell blot analysis revealed the presence of dominant T‐cell epitopes in the areas of Mr 200 000–75 000 and < 50 000 polypeptides. No response was demonstrated in the Mr 72 000 region (migration site of the major surface antigen), suggesting T‐cell dependent mechanisms are most likely not responsible for the surface antigen switch which occurred during the course of infection. This model infection can be used to study the role of immunological mechanisms in Giardia lamblia variant antigen switching and in the control of infections.
Secretion of the C3 component of complement by peritoneal cells cultured with encapsulated Cryptococcus neoformans

Two isolates of Cryptococcus neoformans were identified as being widely divergent in pathogenic potential after intratracheal infection of mice. These isolates differed in their ability to upregulate capsule synthesis when grown under tissue culture conditions, and this property correlated with virulence. We postulated that differential capsule synthesis may cause differential stimulation of macrophages to produce products such as complement components. To test this hypothesis, heat-killed yeast cells were incubated with normal mouse peritoneal cells (PC) before the level of C3 secreted was determined. Cryptococcal stimulants were grown on mycological agar, which does not promote capsule synthesis, or in RPMI 1640 at 37 degrees C in an atmosphere of 5% CO2, which stimulates capsule synthesis, to determine the role that the capsule plays in the induction of C3 secretion. C3 levels were elevated in cultures containing cryptococci grown in RPMI 1640 at 37 degrees C in an atmosphere of 5% CO2, and the level of C3 detected was correlated with the amount of capsule expressed by the yeast cell stimulant. Nonencapsulated mutants of C. neoformans did not stimulate C3 secretion. Purified capsular polysaccharide (glucuronoxylomannan [GXM]) also stimulated the PC to secrete C3. Two signals were required before GXM stimulated C3 secretion. The second signal was identified as endotoxin present in small amounts (0.06 ng per ml) in tissue medium. Endotoxin may provide a priming stimulus for PC to express receptors or other cytokines needed for effective stimulation of C3. These experiments show that enhancement of C3 secretion by C. neoformans is due to GXM and is correlated with the virulence of the cryptococcal isolate.
Brain response to complex visual stimuli in Parkinson's patients with hallucinations: A functional magnetic resonance imaging study

Visual hallucinations (VH) in Parkinson's disease (PD) have been associated with gray matter reductions in visual associative areas and with abnormal patterns of brain activation in posterior and frontal regions. However, all previous fMRI studies have used simple visual stimuli. The objective of our study was, therefore, to compare the pattern of brain activation during a one‐back face detection task. We examined 10 PD patients with VH, 10 PD patients without VH, and 10 controls matched for age and education. The fMRI task consisted in three blocks of 21‐face stimuli (activation condition) and three blocks of 21‐colored mosaics (control condition). Subjects were asked to press a key when two identical stimuli were presented consecutively. During the face condition, compared with patients without VH, hallucinating PD patients showed significant reductions in the activation of several right prefrontal areas, such as the inferior (BA 10,47), superior (BA 6/8), middle frontal (BA 8), and anterior cingulate gyrus (BA 31/32). In the control condition, we found a hyperactivation in the hallucinating PD sample compared with the nonVH patients in the right inferior frontal gyrus. A dysfunction of the frontal areas associated with the control of attention could predispose to VH through an abnormal processing of relevant and irrelevant visual stimuli. © 2008 Movement Disorder Society
MiR-22-3p Regulates Cell Proliferation and Inhibits Cell Apoptosis through Targeting the eIF4EBP3 Gene in Human Cervical Squamous Carcinoma Cells

Background: MicroRNAs (miRNAs) are non-coding small RNAs that function as negative regulators of gene expression and are involved in tumour biology. The eIF4E-binding proteins (eIF4EBPs) play essential roles in preventing translation initiation and inhibiting protein synthesis at a global or message-specific level in a variety of tumours. Methods: According to comparative miRNA profiles of clinical cervical cancer and non-cancerous cervical tissue specimens, several miRNAs were aberrantly expressed in the cervical cancer samples. C33a and SiHa cell proliferation and apoptosis were detected using methyl thiazolyl tetrazolium (MTT) and flow cytometry assays, respectively. Results: Among the aberrantly expressed miRNAs, miR-22-3p was significantly differentially expressed in cervical cancer tissues and was highly associated with cervical cancer cell growth regulation. In addition, bioinformatic predictions and experimental validation were used to identify whether eIF4E-binding protein 3 (eIF4EBP3) was a direct target of miR-22-3p; eIF4EBP3 protein levels were generally low in the cervical cancer tissues. Furthermore, functional studies revealed that either a miR-22-3p inhibitor or eIF4EBP3 overexpression could induce apoptosis in cervical cancer cells in vitro. Importantly, we found that eIF4EBP3 accumulation could significantly attenuate cervical cancer cell proliferation triggered by a miR-22-3p mimic as well as enhance apoptosis in cervical cancer cells. Conclusion: Taken together, our data provide primary proof that miR-22-3p can induce cervical cancer cell growth at least in part by up-regulating its expression to decrease eIF4EBP3 expression levels; miR-22-3p thus holds promise as a prognostic biomarker and potential therapeutic target for treating cervical cancer.
Job control, job demands, or social class? The impact of working conditions on the relation between social class and health

Background: The aim of the study was to investigate (1) how much of the association between health and social class is accounted by psychosocial working conditions, and (2) whether health is related to working conditions after controlling for social class. Methods: The data derive from the surveys of the Helsinki health study, collected in 2000, 2001, and 2002 from 40–60 year old employees working for the City of Helsinki (n = 8970, response rate 67%). The study measured occupation based social class and Karasek’s demand-control model. The health outcomes were self rated health as less than good and limiting longstanding illness. Age adjusted prevalence percentages and fitted logistic regression models were calculated. Results: The individual effects of social class and psychosocial working conditions on self rated health and limiting longstanding illness were strong among both men and women. The relation between social class and both health outcomes considerably attenuated when job control was controlled for, but was reinforced when controlling for job demands. Controlling for both job control and job demands attenuated the relation between social class and self rated health and limiting longstanding illness among women, however, was reinforced among men. Conclusions: A substantial part of the relation between social class and health could be attributed to job control, however, job demands reinforced the relation. Although the effect of social class is mediated by psychosocial working conditions, both social class and working conditions were related to health after mutual adjustments.
Splenic RNA and MicroRNA Mimics Promote Complement Factor B Production and Alternative Pathway Activation via Innate Immune Signaling

Complement factor B (cfB) is an essential component of the alternative pathway (AP) and plays an important role in the pathogenesis of polymicrobial sepsis. However, the mechanism leading to cfB production and AP activation during sepsis remains poorly understood. In this study, we found that plasma cell–free RNA was significantly increased following cecal ligation and puncture (CLP), an animal model of polymicrobial sepsis, and was closely associated with sepsis severity. Quantitative RT-PCR and microRNA (miRNA) array analysis revealed an increase in bacterial RNA and multiple host miRNAs (miR-145, miR-146a, miR-122, miR-210) in the blood following CLP. Treatment with tissue RNA or synthetic miRNA mimics (miR-145, miR-146a, miR-122, miR-34a) induced a marked increase in cfB production in cardiomyocytes or macrophages. The newly synthesized cfB released into medium was biologically active because it participated in AP activation initiated by cobra venom factor. Genetic deletion of TLR7 or MyD88, but not TLR3, and inhibition of the MAPKs (JNK and p38) or NF-κB abolished miR-146a–induced cfB production. In vivo, CLP led to a significant increase in splenic cfB expression that correlated with the plasma RNA or miRNA levels. Peritoneal injection of RNA or miR-146a led to an increase in cfB expression in the peritoneal space that was attenuated in MyD88-knockout or TLR7-knockout mice, respectively. These findings demonstrate that host cellular RNA and specific miRNAs are released into the circulation during polymicrobial sepsis and may function as extracellular mediators capable of promoting cfB production and AP activation through specific TLR7 and MyD88 signaling.
Fyn Is Required for Haloperidol-induced Catalepsy in Mice*

Fyn-mediated tyrosine phosphorylation of N-methyl-d-aspartate (NMDA) receptor subunits has been implicated in various brain functions, including ethanol tolerance, learning, and seizure susceptibility. In this study, we explored the role of Fyn in haloperidol-induced catalepsy, an animal model of the extrapyramidal side effects of antipsychotics. Haloperidol induced catalepsy and muscle rigidity in the control mice, but these responses were significantly reduced in Fyn-deficient mice. Expression of the striatal dopamine D2 receptor, the main site of haloperidol action, did not differ between the two genotypes. Fyn activation and enhanced tyrosine phosphorylation of the NMDA receptor NR2B subunit, as measured by Western blotting, were induced after haloperidol injection of the control mice, but both responses were significantly reduced in Fyn-deficient mice. Dopamine D2 receptor blockade was shown to increase both NR2B phosphorylation and the NMDA-induced calcium responses in control cultured striatal neurons but not in Fyn-deficient neurons. Based on these findings, we proposed a new molecular mechanism underlying haloperidol-induced catalepsy, in which the dopamine D2 receptor antagonist induces striatal Fyn activation and the subsequent tyrosine phosphorylation of NR2B alters striatal neuronal activity, thereby inducing the behavioral changes that are manifested as a cataleptic response.
Nils Rosén von Rosenstein and neonatal jaundice in the 18th century.

BACKGROUND Nils Rosén von Rosenstein (1706-1773) was a Swedish nobleman and a professor at Uppsala University. His series of lectures on children's diseases and their treatment was published in 1764 under the title Underrättelser om Barn-Sjukdomar och Deras Bote-Medel. MATERIALS AND METHODS Rosén von Rosenstein's book was translated into several languages. The present paper deals with the opinions and advice proffered on the jaundiced neonate in chapter 25 of the Danish edition from 1769. RESULTS The distinction between jaundice in the neonate and jaundice in older children is not clear everywhere in the chapter, and much of Rosén von Rosenstein's advice on therapy appears to be intended for all age groups. Rosén von Rosenstein believed that neonatal jaundice was less common in Sweden than elsewhere, and ascribed this to the common practice of purging newborns with a manna sugar laxative. The principal cause of jaundice, according to Rosén von Rosenstein, was bile stasis. When milk curdled in the stomach, the curds could plug the common bile duct, and bile would be forced into the lymphatics and from there into the blood. Thus, the bile was carried around the body and caused the skin and the sclera, as well as other organs, to become yellow. Cure was usually easy-a laxative in the form of puréed manna with powdered rhubarb was what Rosén von Rosenstein recommended. CONCLUSION Rosén von Rosenstein's opinions and advice concerning neonatal jaundice were not original, and did not differ from those found in other medical texts from the 18th and 19th centuries. The bile stasis explanation for all kinds of jaundice, including neonatal jaundice, was widely held in the 18th century, and continued to predominate in paediatric texts until the end of the 19th century. Similarly, laxatives and enemas as the cure-all for many ailments held sway until the late 1800s.