Miracle-dz/UniFAR-FTUs huggingface dataset:
Accelerated diabetes in rat insulin promoter-tumor necrosis factor-alpha transgenic nonobese diabetic mice lacking major histocompatibility class II molecules.

The major predisposing genetic component in type 1 diabetes maps to the major histocompatibility complex locus in both mice and humans. To verify the HLA class II association with disease pathogenesis, we adopted the transgenic approach. Expression of HLA-DQ8, the molecule showing the strongest association with human type 1 diabetes, in the diabetes-predisposing milieu of NOD mice in the absence of the endogenous class II molecule I-A(g7) did not render susceptibility to type 1 diabetes. To study if providing a local proinflammatory environment would lead to diabetes in these mice, Abeta(o). NOD.DQ8 were bred with C57BL/6 mice expressing tumor necrosis factor (TNF)-alpha in the beta-cells of the islets of Langerhans. Surprisingly, although diabetes was evident in the F1 intercross expressing rat insulin promoter (RIP)-TNF, offspring lacking either endogenous or transgenic class II molecules developed accelerated diabetes with high frequency in both sexes. Moreover, expression of any functional class II molecule seemed to confer significant protection from diabetes in this model. Thus, neonatal expression of TNF-alpha in an islet-specific manner bypassed the requirement of CD4(+) T-cells and resulted in diabetes that could be mediated by CD8(+) T-cells. We also show for the first time that diabetes in NOD.RIP-TNF mice can occur independent of inheritance of NOD-derived idd1.
Escherichia coli O 157 : H 7-Prevalence and Risk Factors of Infection in Edo State , Nigeria

We determined the prevalence of Escherichia coli O157:H7 as well as risks factors of infection in Edo State, Nigeria. One thousand (1000) fecal specimens from consenting persons from both sexes and of all age groups within the 3 Senatorial districts, reporting with cases of diarrhea and other gastrointestinal complaints as well as apparently healthy individuals, were inoculated onto MacConkey, Sorbitol MacConkey, Eosin Methylene Blue and Blood agar. Media were incubated aerobically at 37C for 24 hr. Isolates were identified using standard microbiological techniques. For the study data, Chi-square (χ) or Fisher’s exact test as appropriate and odd ratio analysis were done using the statistical software INSTAT®. A 2.7% rate of infection was recorded. Most of the isolates were recovered from subjects living within the bustling commercial city of the state where access to fast-food and road side restaurants is common. Other favorable factors found to be associated with infection included diarrhea as clinical symptoms, the wetter seasons of the year and asymptomatic carriage of infection. Gender and age were not statistically significant (p˃ 0.05) risk factors of infection in this study.
Facteurs influençant la localisation du foramen mandibulaire

L’anesthesie du nerf alveolaire inferieur est l’un des actes dentaires les plus frequents. Elle est obtenue par injection au niveau du foramen mandibulaire. La position de ce dernier ne peut etre estimee cliniquement que par rapport au plan d’occlusion. Le but de cette these, grâce a une etude transversale et une longitudinale, est d’evaluer la distance entre le foramen et le plan d’occlusion et les facteurs l’influencant. Des radiographies cephalometriques laterales de 145 patients qui ont subi un traitement orthodontique ont ete utilisees. Des variables cephalometriques avant le debut et 10 ans apres la fin du traitement orthodontique (pour 50 d’entre eux) ont ete analysees. Avec l’âge (croissance) et chez les patients avec une hauteur faciale diminuee (morphologie faciale de type « short-face »), la distance foramen-plan d’occlusion augmente. Ces facteurs devraient donc etre pris en compte afin d’obtenir une anesthesie efficace du nerf alveolaire inferieur.
Enhanced expression of B7‐1, B7‐2, and intercellular adhesion molecule 1 in sinusoidal endothelial cells by warm ischemia/reperfusion injury in rat liver

To elucidate a role of costimulatory molecule and cell adhesion molecule in hepatic ischemia/reperfusion injury, we examined an alteration in B7‐1 (CD80), B7‐2 (CD86), and intercellular adhesion molecule 1 (ICAM‐1; CD54) expression in the rat liver after warm ischemia/reperfusion injury. To induce hepatic warm ischemia in a rat model, both portal vein and hepatic artery entering the left‐lateral and median lobes were occluded by clamping for 30 minutes or 60 minutes, and then reperfused for 24 hours. B7‐1, B7‐2, and ICAM‐1 expressions in the liver were analyzed by immunofluorescence staining and real‐time reverse transcription polymerase chain reaction (RT‐PCR). Although B7‐1 and B7‐2 expressions were at very low levels in the liver tissues from normal or sham‐operated control rats, both B7‐1 and B7‐2 expressions were enhanced at protein and messenger RNA (mRNA) levels in the affected, left lobes after warm ischemia/reperfusion. ICAM‐1 protein and mRNA were constitutively expressed in the liver of normal and sham‐operated control rats, and further up‐regulated after warm ischemia/reperfusion. Localization of increased B7‐1, B7‐2, and ICAM‐1 proteins, as well as von Willebrand factor as a marker protein for endothelial cells, was confined by immunofluorescence staining to sinusoidal endothelial cells in hepatic lobules. Data from quantitative real‐time RT‐PCR analysis revealed that B7‐1 and B7‐2 mRNA levels were elevated in hepatic lobes after warm ischemia/reperfusion (5.13‐ and 52.9‐fold increase, respectively), whereas ICAM‐1 mRNA expression was rather constitutive but further enhanced by warm ischemia/reperfusion (4.24‐fold increase). These results suggest that hepatic sinusoidal endothelial cells play a pivotal role as antigen‐presenting cells by expressing B7‐1 and B7‐2 in warm hepatic ischemia/reperfusion injury, and that B7‐1 and/or B7‐2 might be the primary target to prevent early rejection and inflammatory reactions after hepatic ischemia/reperfusion injury associated with liver transplantation.
Assessment of the diagnostic accuracy of double inversion recovery sequence compared with FLAIR and T2W_TSE in detection of cerebral multiple sclerosis lesions

Background Multiple sclerosis (MS) is a demyelinating disease of the central nervous system. MRI has an important role in early diagnosis of MS within diagnostic criteria. Aim To determine the diagnostic value of the double inversion recovery (DIR) sequence in detection of brain MS lesions. Methods In this cross-sectional study, 55 patients were admitted to the MRI department in Vali-E-Asr Hospital in Qaemshahr, Iran, from May 2016 to February 2016. Imaging was performed on a 1.5T Philips MR system using DIR, fluid attenuated inversion recovery (FLAIR), and T2-weighted turbo spin echo (T2W_TSE) sequences with the same parameters, including field of view (FOV), matrix, slice thickness, voxel size, and number of signal averaging (NSA). The DIR sequence has two different time inversions (TI1=3400, TI2=325ms): suppressing cerebrospinal fluid (CSF) and white matter signal. Data analysis was performed using the SPSS version 20, and p-value was gained from the patient-wise analysis by Wilcoxon analysis and paired samples t-test for matched pairs. Results More lesions in number and size were depicted on the DIR sequence compared with FLAIR (p=0.000 with a relative ratio of 6) and T2W_TSE (p=0.000 with a relative ratio of 10). DIR demonstrated significantly more intracortical lesions compared with FLAIR (p=0.000 with a relative ratio of 2.53) and T2W_TSE (p=0.000 and relative ratio of 8.87). There was significantly higher contrast ratio between the white matter lesions and the normal appearing white matter (NAWM) in all anatomical regions especially in deep white matter (p=0.001). Conclusion An increasing total number of MS lesions can be detected by DIR sequence; thus, we recommend adding DIR sequence in routine MR protocols for MS patients.
Mechanism of 3‐nitropropionic acid‐induced membrane permeability transition of isolated mitochondria and its suppression by L‐carnitine

3‐Nitropropionic acid (3NP) functions as an irreversible inhibitor of succinic acid dehydrogenase (complex II) and induces neuronal disorders in rats similar to those in patients with Huntington's disease. It is well known that L‐carnitine (LC), a carrier of long chain fatty acid into the mitochondrial matrix, attenuates the neuronal degeneration in 3NP‐treated rats. From these findings it has been suggested that 3NP induces certain neuronal cell death through mitochondrial dysfunction and that LC preserves the neurons against the dysfunction of mitochondria caused by 3NP. However, the detailed mechanism of cell death by 3NP and the protective actions of LC against the mitochondrial dysfunction have not been fully elucidated yet. Thus, we studied the molecular mechanism of the effects of 3NP and LC on isolated rat liver mitochondria. 3NP inhibited succinate respiration and the decreased respiratory control ratio of isolated mitochondria without affecting oxidative phosphorylation. 3NP induced a membrane permeability transition (MPT), which plays an important role in the mechanism of apoptotic cell death. 3NP stimulated Ca2+ release from mitochondria, decreased membrane potential, induced mitochondrial swelling, and stimulated cytochrome c release from mitochondria. 3NP‐induced swelling was suppressed by bovine serum albumin, inhibitors of phospholipase A2 and by an inhibitor of classic MPT, cyclosporin A. Furthermore, LC suppressed the changes brought about by 3NP in mitochondrial functions in the presence of ATP. These results suggest that MPT underlies the mechanism of 3NP‐induced cell death, and that LC attenuates mitochondrial MPT by decreasing long chain fatty acids generated by phospholipase A2. Copyright © 2008 John Wiley & Sons, Ltd.
Hypothalamic and plasma total nitrate/nitrite concentrations in spontaneously hypertensive rats

Stable end‐products of nitric oxide (NO) metabolism, nitrates and nitrites, were measured in hypothalamic extracts and plasma samples of Okamoto spontaneously hypertensive (SH) rats. The mean total nitrate/nitrite concentration was significantly lower in the hypothalami of SH rats compared with the normotensive Wistar Kyoto (WKY) control animals (P < 0.01). In contrast, their plasma concentrations were significantly higher (P < 0.05). These results indicate that the hypertensive state in SH rats is associated with a diminished production of hypothalamic NO, while the raised plasma nitrate/nitrite levels could reflect an increased compensatory endothelial NO synthase activity in these animals compared with the WKY controls.
Cerebral Microbleeds in Patients with Dementia with Lewy Bodies and Parkinson Disease Dementia

BACKGROUND AND PURPOSE: The burden of amyloid β is greater in patients with dementia with Lewy bodies than in those with Parkinson disease dementia, and an increased amyloid β load is closely related to a higher incidence of cerebral microbleeds. Here, we investigated the prevalence and topography of cerebral microbleeds in patients with dementia with Lewy bodies and those with Parkinson disease dementia to examine whether cerebral microbleeds are more prevalent in patients with dementia with Lewy bodies than in those with Parkinson disease dementia. MATERIALS AND METHODS: The study population consisted of 42 patients with dementia with Lewy bodies, 88 patients with Parkinson disease dementia, and 35 controls who underwent brain MR imaging with gradient recalled-echo. Cerebral microbleeds were classified as deep, lobar, or infratentorial. RESULTS: The frequency of cerebral microbleeds was significantly greater in patients with dementia with Lewy bodies (45.2%) than in those with Parkinson disease dementia (26.1%) or in healthy controls (17.1%; P = .017). Lobar cerebral microbleeds were observed more frequently in the dementia with Lewy bodies group (40.5%) than in the Parkinson disease dementia (17%; P = .004) or healthy control (8.6%; P = .001) group, whereas the frequencies of deep and infratentorial cerebral microbleeds did not differ among the 3 groups. Logistic regression analyses revealed that, compared with the healthy control group, the dementia with Lewy bodies group was significantly associated with the presence of lobar cerebral microbleeds after adjusting for age, sex, nonlobar cerebral microbleeds, white matter hyperintensities, and other vascular risk factors (odds ratio, 4.39 [95% CI, 1.27–15.25]). However, compared with the healthy control group, the Parkinson disease dementia group was not significantly associated with lobar cerebral microbleeds. CONCLUSIONS: This study showed that patients with dementia with Lewy bodies had a greater burden of cerebral microbleeds and exhibited a lobar predominance of cerebral microbleeds than did patients with Parkinson disease dementia.
Lymphotoxin- (cid:1) and TNF Have Essential but Independent Roles in the Evolution of the Granulomatous Response in Experimental Leprosy

Recent studies identified an association between genetic variants in the lymphotoxin- (cid:1) (LT (cid:1) ) gene and leprosy. To study the influence of LT (cid:1) on the control of experimental leprosy, both low- and high-dose Mycobacterium leprae foot pad (FP) infections were evaluated in LT (cid:1) -deficient chimeric (cLT (cid:1) (cid:2) / (cid:2) ) and control chimeric (cB6) mice. Cellular responses to low-dose infection in cLT (cid:1) (cid:2) / (cid:2) mice were dramatically different, with reduced accumulation of CD4 (cid:3) and CD8 (cid:3) lymphocytes and macrophages and failure to form granulomas. Growth of M. leprae was contained for 6 months, but augmented late in infection. In contrast, tumor necrosis factor knockout and tumor necrosis factor receptor 1 knockout FPs exhibited extensive inflammatory infiltration with an increase in M. leprae growth throughout infection. Following high-dose infection, cB6 FP induration peaked at 4 weeks and was maintained for 12 weeks. Induration was not sustained in
Workplace heat stress, health and productivity – an increasing challenge for low and middle-income countries during climate change

Background: Global climate change is already increasing the average temperature and direct heat exposure in many places around the world. Objectives: To assess the potential impact on occupational health and work capacity for people exposed at work to increasing heat due to climate change. Design: A brief review of basic thermal physiology mechanisms, occupational heat exposure guidelines and heat exposure changes in selected cities. Results: In countries with very hot seasons, workers are already affected by working environments hotter than that with which human physiological mechanisms can cope. To protect workers from excessive heat, a number of heat exposure indices have been developed. One that is commonly used in occupational health is the Wet Bulb Globe Temperature (WBGT). We use WBGT to illustrate assessing the proportion of a working hour during which a worker can sustain work and the proportion of that same working hour that (s)he needs to rest to cool the body down and maintain core body temperature below 38°C. Using this proportion a ‘work capacity’ estimate was calculated for selected heat exposure levels and work intensity levels. The work capacity rapidly reduces as the WBGT exceeds 26–30°C and this can be used to estimate the impact of increasing heat exposure as a result of climate change in tropical countries. Conclusions: One result of climate change is a reduced work capacity in heat-exposed jobs and greater difficulty in achieving economic and social development in the countries affected by this somewhat neglected impact of climate change.
Dysregulation of the sympathetic nervous system, hypothalamic-pituitary-adrenal axis and executive function in individuals at risk for suicide.

BACKGROUND Suicidal behaviour aggregates in families, and the hypothalamic-pituitary-adrenal (HPA) axis and noradrenergic dysregulation may play a role in suicide risk. It is unclear whether stress dysregulation is a heritable trait of suicide or how it might increase risk. We investigated stress reactivity of the autonomic nervous system and the HPA axis in suicide predisposition and characterized the effect of this dysregulation on neuropsychologic function. METHODS In this family-based study of first-degree relatives (n = 14) of suicide completers and matched controls with no family or personal history of suicidal behaviour (n = 14), participants underwent the Trier Social Stress Test (TSST). We used salivary α-amylase and cortisol levels to characterize stress reactivity and diurnal variation. We administered a series of neuropsychologic and executive function tests before and after the TSST. RESULTS Despite normal diurnal variation, relatives of suicide completers exhibited blunted cortisol and α-amylase TSST reactivity. Although there were no baseline differences in conceptual reasoning, sustained attention or executive function, the relatives of suicide completers did not improve on measures of inhibition upon repeated testing after TSST. Secondary analyses suggested that these effects were related to suicide vulnerability independent of major depression. LIMITATIONS The sample size was small, and the design prevents us from disentangling our findings from the possible traumatic consequences of losing a relative by suicide. CONCLUSIONS Blunted stress response may be a trait of suicide risk, and impairment of stress-induced executive function may contribute to suicide vulnerability.
Fault tolerant control strategy based on actuation switch mechanism for more-electric aircraft with vertical tail damage

This paper proposes a fault tolerant control strategy with an actuation switch mechanism for different degrees of vertical tail damage of more-electric aircraft (MEA). A damage degree coefficient of vertical tail is introduced and the relationship between lateral derivatives and damage degree is formulated. Benefit from the more-electric characteristics, a combination of electro-hydrostatic actuation (EHA) system and engine differential thrust is proposed for serious vertical tail damage to regain lateral-directional stability and manoeuvrability. Furthermore, the reconfigurable control law is carried out by the model reference control (MRC) combined with linear quadratic regulator (LQR). Simulation results with the NASA generic transportation model (GTM) demonstrate the effectiveness of the proposed control strategy for the damaged aircraft.
Genetic evaluation of carcass traits in Japanese quail using ultrasonic and morphological measurements

Abstract 1. A study was conducted to evaluate the carcass composition of 1083 live birds using ultrasonic and morphological measurements and to estimate the genetic relationship between predicted and dissected carcass composition in Japanese quail. 2. Birds were reared for 35 d, and morphological measurements consisting of the length and width of breast muscle were recorded for all birds using a digital caliper. After slaughtering, the weight and percentage of carcass traits were measured on chilled carcasses. The dimensions of breast muscle were measured in 638 birds with an ultrasound scanner before slaughter at 35 d of age. 3. Genetic parameters from univariate and bivariate analyses were obtained by restricted maximum likelihood using ASREML software. 4. Genetic correlations between body weight at 35 d (BW35) and the percentage of carcass traits were low. Therefore, selection for BW35 may not effectively improve the yield of carcass components in Japanese quail. 5. High genetic correlations between carcass traits and ultrasonic measurements compared to morphological measurements suggest that the ultrasonic technique is a better method to improve breast weight and yield in Japanese quail.
Pre‐ and postsynaptic whole‐cell recordings in the medial nucleus of the trapezoid body of the rat.

1. Simultaneous whole‐cell recordings in a rat brain slice preparation are described from presynaptic terminals (calyces of Held) and postsynaptic somata which form an axosomatic synapse in the medial nucleus of the trapezoid body (MNTB). 2. Presynaptic action potentials evoked suprathreshold excitatory postsynaptic potentials (EPSPs). The minimum synaptic delay was around 0.4 ms at 36 degrees C and 0.9 ms at 23‐24 degrees C. The amplitude of the L‐alpha‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionate (AMPA) receptor‐mediated component of the excitatory postsynaptic currents (EPSCs) was 2‐13 nA (at ‐80 mV). 3. Current‐voltage relations showed that presynaptic Ca2+ channels were of the high voltage‐activated type. 4. A single action potential evoked a presynaptic fluorescence transient that decayed with a time constant of 0.3‐0.7 s, depending on the concentration (60‐200 microM) of the Ca2+ indicator Calcium Green‐5N (CG‐5N). The peak amplitude of the [Ca2+]i transient was severalfold larger in the terminal than in the preterminal axon. 5. EPSC peak amplitudes were stable for more than 30 min after establishing the whole‐cell configuration in the presynaptic terminal when the pipette contained 50 microM BAPTA. In contrast, with 1 mM BAPTA, peak amplitudes of EPSCs were reduced to one‐third. 6. Trains of presynaptic action potentials evoked EPSCs with progressively smaller amplitudes. Little change was observed in the depression when the terminals were dialysed with 50 microM BAPTA, whereas depression was reduced with 1 mM BAPTA. 7. In low (1 mM) [Ca2+]o, facilitation instead of depression of EPSCs was observed. 8. The effects of presynaptic BAPTA suggest that the endogenous mobile Ca2+ buffer capacity of giant presynaptic terminals in the MNTB is lower than in other terminals of fast transmitting synapses.
Phospholipase C (cid:1) Modulates (cid:2) -Adrenergic Receptor Dependent Cardiac Contraction and Inhibits Cardiac Hypertrophy

—Phospholipase C (PLC) (cid:1) is a recently identified enzyme regulated by a wide range of molecules including Ras family small GTPases, Rho A, G (cid:2) 12/13 , and G (cid:3)(cid:4) with primary sites of expression in the heart and lung. In a screen for human signal transduction genes altered during heart failure, we found that PLC (cid:1) mRNA is upregulated. Two murine models of cardiac hypertrophy confirmed upregulation of PLC (cid:1) protein expression or PLC (cid:1) RNA. To identify a role for PLC (cid:1) in cardiac function and pathology, a PLC (cid:1) -deficient mouse strain was created. Echocardiography indicated PLC (cid:1) (cid:1) / (cid:1) mice had decreased cardiac function, and direct measurements of left ventricular contraction demonstrated that PLC (cid:1) (cid:1) / (cid:1) mice had a decreased contractile response to acute isoproterenol administration. Cardiac myocytes isolated from PLC (cid:1) (cid:1) / (cid:1) mice had decreased (cid:3) -adrenergic receptor ( (cid:3) AR)-dependent increases in Ca 2 (cid:2) transient amplitudes, likely accounting for the contractile deficiency in vivo. This defect appears to be independent from the ability of the (cid:3) AR system to produce cAMP and regulation of sarcoplasmic reticulum Ca 2 (cid:2) pool size. To address the significance of these functional deficits to cardiac pathology, PLC (cid:1) (cid:1) / (cid:1) mice were subjected to a chronic isoproterenol model of hypertrophic stress. PLC (cid:1) (cid:1) / (cid:1) mice were more susceptible than wild-type littermates to development of hypertrophy than wild-type littermates. Together, these data suggest a novel PLC-dependent component of (cid:3) AR signaling in cardiac myocytes responsible for maintenance of maximal contractile reserve and loss of PLC (cid:1) signaling sensitizes the heart to development of hypertrophy in response to chronic cardiac stress. ( Circ Res . 2005;97:0-0.)