Miracle-dz/UniFAR-FTUs huggingface dataset:
Women in hospital medicine in the United Kingdom: glass ceiling, preference, prejudice or cohort effect?

OBJECTIVE To assess from official statistics whether there is evidence that the careers of women doctors in hospitals do not progress in the same way as those of men. DESIGN The proportions of female hospital doctors overall (1963–96), and in the specialties of medicine, surgery, obstetrics and gynaecology, pathology, radiology/radiotherapy, anaesthetics and psychiatry (1974–1996) were examined. Additionally data were examined on career preferences and intentions from pre-registration house officers, final year medical students, and medical school applicants (1966–1991). ANALYSIS Data were analysed according to cohort of entry to medical school to assess the extent of disproportionate promotion. RESULTS The proportion of women in hospital career posts was largely explained by the rapidly increasing proportion of women entering medical school during the past three decades. In general there was little evidence for disproportionate promotion of women in hospital careers, although in surgery, hospital medicine and obstetrics and gynaecology, fewer women seemed to progress beyond the SHO grade, and in anaesthetics there were deficits of women at each career stage. Analyses of career preferences and intentions suggest that disproportionate promotion cannot readily be explained as differential choice by women. CONCLUSIONS Although there is no evidence as such of a “glass ceiling” for women doctors in hospital careers, and the current paucity of women consultants primarily reflects historical trends in the numbers of women entering medical school, there is evidence in some cases of disproportionate promotion that is best interpreted as direct or indirect discrimination.
Monocytes Expand with Immune Dysregulation and Is Associated with Insulin Resistance in Older Individuals with Chronic HIV

Background Rates of insulin resistance are increased in HIV-infected patients on stable antiretroviral therapy (ART). Such increase may partially be due to HIV-induced immune dysregulation involving monocytes (MO) and its subsets. Materials and Methods Cross-sectional analysis of 141 HIV-infected subjects age ≥ 40 years on stable ART. Homeostatic model assessment–insulin resistance (HOMA-IR) and rates of metabolic syndrome were calculated. Subjects were classified by fasting glucose and oral glucose tolerance test (OGTT) into clinical diabetes categories. Multi-parametric flow cytometry was used to determine MO subset percentages: [classical (CD14++CD16−), intermediate (CD14++CD16+), non-classical (CD14low/+CD16++), and a recently identified fourth (CD14low/+CD16−) ‘transitional’ MO subset] and percentage of activated (CD38+HLA-DR+) CD8 T cells. Absolute levels of cells were calculated using clinical CBC and T cell subset data. Multiple plasma soluble biomarkers were assessed by Luminex technology. Results Median age 50 years, CD4 count (percent) 505 cells/µL (29%), and 89% male. Total MO (r = −0.23, p = 0.006) and classical and non-classical MO subsets correlated negatively with CD4 percent. No correlations were seen with CD4 count as absolute values. Log-total MO and log-classical MO predicted HOMA-IR independently of HIV immuno-virologic and diabetes risk factors (β = 0.42, p = 0.02 and β = 0.35, p = 0.02, respectively) and were increased in subjects with metabolic syndrome (p = 0.03 and p = 0.05 respectively). Total and/or subset MO levels correlated with multiple soluble plasma biomarkers including CRP, IL-6, MMP-9, MPO, SAA, SAP and tPAI-1, with tPAI-1 independently predicting HOMA-IR (β = 0.74, p<0.001). Conclusions MO levels increase with worsening HIV immune dysregulation as assessed by CD4 percent. CD4 percent may provide additional information about MO and metabolic risk in this population beyond absolute values. MO, and specifically classical MO, may contribute to insulin resistance and metabolic syndrome during chronic HIV infection. Multiple soluble plasma biomarkers including tPAI-1 increase with increase in MO. Levels of tPAI-1 independently predict the development of insulin resistance.
Information-Geometric Measure for Neural Spikes

This study introduces information-geometric measures to analyze neural firing patterns by taking not only the second-order but also higher-order interactions among neurons into account. Information geometry provides useful tools and concepts for this purpose, including the orthogonality of coordinate parameters and the Pythagoras relation in the Kullback-Leibler divergence. Based on this orthogonality, we show a novel method for analyzing spike firing patterns by decomposing the interactions of neurons of various orders. As a result, purely pairwise, triple-wise, and higher-order interactions are singled out. We also demonstrate the benefits of our proposal by using several examples.
High urinary concentrations of activin A in asphyxiated full-term newborns with moderate or severe hypoxic ischemic encephalopathy.

BACKGROUND Hypoxic ischemic encephalopathy (HIE) is a major cause of permanent neurological disabilities in full-term newborns. We measured activin A in urine collected immediately after birth in asphyxiated full-term newborns, and assessed the ability of the measurements to predict the occurrence of perinatal encephalopathy. METHODS We studied 30 infants with perinatal asphyxia and 30 healthy term neonates at the same gestational age. We recorded routine laboratory variables, cranial assessments by standard cerebral ultrasound, and the presence or absence of neurological abnormalities during the first 7 days after birth. Urinary activin A concentrations were measured at first urination and 12, 24, 48, and 72 h after birth. RESULTS Asphyxiated infants were subdivided as follows: group A (n = 18): no or mild HIE with good prognosis and group B (n = 12): moderate or severe HIE with a greater risk of neurological handicap. Activin A concentrations in urine collected at birth (median collection time at first urination <2 h) and at 12, 24, 48, and 72 h from birth were significantly (P <0.0001) higher in asphyxiated newborns with moderate or severe HIE (Group B) than in those with absent of mild HIE (group A) and controls. Concentrations did not differ between group A and controls. Activin A concentrations were >0.08 mug/L at first urination in 10 of 12 patients with moderate or severe HIE but in none of 18 patients with no or mild HIE. CONCLUSIONS Activin A measurements in urine soon after birth may be a promising tool to identify which asphyxiated infants are at risk of neurological sequelae.
Studies of apoptosis in breast cancer

Breast cancer is the commonest malignancy in women and comprises 18% of all cancers in women. The United Kingdom has the highest age standardised incidence and mortality from breast cancer in the world.1 Since 1990, death rates from breast cancer have decreased by over 25%, and this is at least in part due to the improved use of adjuvant tamoxifen and chemotherapy. Current research is focused on a greater understanding of the response and resistance to treatment, including the role of apoptosis. Accessibility of the primary tumour makes breast cancer uniquely suitable for such studies. Here we summarise and integrate the data on apoptosis and its role in the development, prognosis, and treatment of breast cancer. Normal breast development is controlled by a balance between cell proliferation and apoptosis, and there is strong evidence that tumour growth is not just a result of uncontrolled proliferation but also of reduced apoptosis. The balance between proliferation and apoptosis is crucial in determining the overall growth or regression of the tumour 2 3 in response to chemotherapy, radiotherapy and, more recently, hormonal treatments. All of these act in part by inducing apoptosis.4–6 Thus it is possible to delineate the biology of individual tumours at the molecular and biochemical level by examining apoptosis and its control and regulation and to exploit these to clinical advantage. Much of this work is still the subject of research. Understanding these relations could allow individually tailored treatments to maximise tumour regression and the efficacy of treatment. It could also help to answer why some tumours fail to respond and thereby indicate new routes of drug development. #### Summary points Increased apoptosis with increased proliferation is associated with malignant tumours Breast tumours with increased apoptosis are more likely to be high grade and negative for oestrogen receptors High …
Multi-Conditional Learning: Generative/Discriminative Training for Clustering and Classification

This paper presents multi-conditional learning (MCL), a training criterion based on a product of multiple conditional likelihoods. When combining the traditional conditional probability of "label given input" with a generative probability of "input given label" the later acts as a surprisingly effective rerularizer. When applied to models with latent variables, MCL combines the structure-discovery capabilities of generative topic models, such as latent Dirichlet allocation and the exponential family harmonium, with the accuracy and robustness of discriminative classifiers, such as logistic regression and conditional random fields. We present results on several standard text data sets showing significant reductions in classification error due to MCL regularization, and substantial gains in precision and recall due to the latent structure discovered under MCL.
Nonsteroidal Anti-Inflammatory Drugs Potentiate 1-Methyl-4-phenylpyridinium (MPP+)-Induced Cell Death by Promoting the Intracellular Accumulation of MPP+ in PC12 Cells

In this study, we investigated the effects of nonsteroidal anti-inflammatory drugs (NSAIDs) on 1-methyl-4-phenylpyridinium (MPP+)-induced cell death in PC12 cells. Coincubation of PC12 cells with indomethacin, ibuprofen, ketoprofen, or diclofenac, but not aspirin or N-[2-(cyclohexyloxy)-4-nitrophenyl]methanosulfonamide (NS-398), significantly potentiated the MPP+-induced cell death. In contrast, these NSAIDs had no effect on rotenone-induced cell death. The potentiating actions of these NSAIDs were not suppressed by treatment with phenyl-N-butyl-nitrone, a radical scavenger; N-acetyl-l-cysteine, an antioxidant; Ac-DEVD-CHO, a selective caspase-3 inhibitor; or 2-chloro-5-nitro-N-phenylbenzamide (GW9662), a selective antagonist of peroxisome proliferator-activated receptor γ. Furthermore, we observed that DNA fragmentation, which is one of the hallmarks of apoptosis, was not induced by coincubation with MPP+ and NSAIDs. We confirmed that coincubation of PC12 cells with 30 μM MPP+ and 100 μM indomethacin, ibuprofen, ketoprofen, or diclofenac led to a significant increase in the accumulation of intracellular MPP+ compared with incubation with 30 μM MPP+ alone. In addition, these NSAIDs markedly reduced the efflux of MPP+ from PC12 cells. (3-(3-(2-(7-Chloro-2-quinolinyl) ethenyl) phenyl ((3-dimethyl amino-3oxo-propyl) thio) methyl) propanoic acid (MK 571), which is an inhibitor of multidrug resistance proteins (MRPs), mimicked the NSAIDs-induced effects, increasing cell toxicity and promoting the accumulation of MPP+. Moreover, some types of MRPs' mRNA were detected in PC12 cells. These results suggest that some NSAIDs might cause a significant increase in the intracellular accumulation of MPP+ via the suppression of reverse transport by the blockade of MRP, resulting in the potentiation of MPP+-induced cell death.
E.E.G. ABNORMALITIES FROM THE TEMPORAL LOBE STUDIED WITH SPHENOIDAL ELECTRODES

In the last few years applied electrophysiology has played an increasing part in the routine clinical work of many neurological and psychiatric centres. Combined clinical and electrophysiological observations have shown the problem of the epilepsies to be very intricate, and the study of abnormalities of cerebral function related to the initiation and spread of an epileptic seizure still largely awaits development of new techniques. The seizures which Hughlings Jackson (Taylor, 1931) classified in the uncinate group (and which more recent workers have called either "psychomotor" or "temporal lobe" epilepsy) have lately aroused an increasing interest. (The literature is reviewed in papers by Penfield and Jasper, 1954; Hill, 1953 ; Meyers, 1954; Gastaut and others, 1953; Magnus, 1954). Routine clinical electroencephalography has contributed to the study of these types of seizures but only the posterior half or two-thirds of the lateral aspect of the temporal lobe may be explored with scalp electrodes. Anatomical considerations suggest that the activity of the anterior third of the temporal lobe, and particularly that of its inferior and uncal areas, cannot be satisfactorily recorded with electrodes placed on the skin (scalp or zygoma) or even in the pharynx or in the external auditory meatus. The region of the foramen ovale appeared to be a suitable area easily reached, from which to record the activity of the anterior inferior regions of the temporal lobe. Jasper (1949) mentioned the use of needle electrodes in the region of the greater wing of the sphenoid (" ala magna " electrodes) introduced by Kristensens and Reyes (1949). Penfield and Jasper (1954) show an x-ray picture of these electrodes introduced by the anterior approach. The insertion of needles close to the foramen ovale with an anterior approach is, however, a rather elaborate procedure (Penman, 1953) with some risk of entering the cranial cavity through the foramen. In 1951 D. P. Jones showed to the E.E.G. Society records taken with sphenoidal needle electrodes using the lateral approach. Pertuiset and Capdevielle-Arfel (1951) and Kerridge (1952) reported on their experience with similar methods, but in all these communications the technical details and observations are scanty. A simple and safe method with slight modification of those previously mentioned has been followed in examining our series of patients. Needle electrodes are introduced through the skin under the zygomatic arch to the vicinity of the foramen ovale. The method described here has become part of the routine investigation of cases in which on clinical or electroencephalographic (E.E.G.) grounds an " epileptogenic abnormality " of one or both temporal lobes is suspected (Hill, 1953 ; Falconer, Hill, Meyer, Mitchell, and Pond, 1955). This paper presents a summary of our experience of 250 consecutive records obtained from 166 patients using this technique up to June, 1953.
Implantable Stimulator for Epileptic Seizure Suppression With Loading Impedance Adaptability

The implantable stimulator for epileptic seizure suppression with loading impedance adaptability was proposed in this work. The stimulator consisted of the high voltage generator, output driver, adaptor, and switches, can constantly provide the required 40-μA stimulus currents, as the loading impedance varied within 10 kΩ -300 kΩ. The performances of this design have been successfully verified in silicon chip fabricated by a 0.35- μm 3.3-V/24-V CMOS process. The power consumption of this work was only 1.1 mW-1.4 mW. The animal test results with the fabricated chip of proposed design have successfully verified in the Long-Evans rats with epileptic seizures.
Haemoglobin variants among voluntary blood donors in Jos, Nigeria: the implications on blood transfusion.

INTRODUCTION The normal haemoglobin is an efficient transporter of oxygen to the tissues and carbondioxide from tissues to the lungs for elimination. Various abnormal haemoglobin variants including, the sickle cell diseases, have been described with varying sickling tendencies. AIMS This study aimed to determine the haemoglobin variants among voluntary blood donors in Jos. METHOD Records of the age, sex, Haemoglobin level, and the haemoglobin genotype of all voluntary blood donors who donated blood at the National Blood Transfusion Service Centre, Jos, Nigeria between January 2011 and April 2012; and their haemoglobin levels and protein electrophoresis determined, were reviewed. RESULTS A total of 937 blood donors, 658 (70.23%) males and 279 (29.79%) females, mean age 32.4 years, donated blood voluntarily, their haemoglobin electrophoretic patterns determined by alkaline cellulose acetate electrophoresis. Donor blood haemoglobin levels were determined by automation. Haemoglobin protein electrophoretic patterns identified among our donors were 77.70% AA, 21.88% AS, 0.22% SC, 0.11% AC and 0.11% SS. Mean haemoglobin levels of the donors according to their haemoglobin proteins electrophoretic patterns were, 150.4 +/- 12.5 gms/l for AA, 151.9 +/- 13.8 gms/l for AS and 131.1 +/- 5.0 gms/l for haemoglobin SC. CONCLUSION Determination of haemoglobin protein electrophoretic patterns of blood unit for transfusion could enhance selective blood issuing based on recipient's haemoglobin type.
Myosin V and the endoplasmic reticulum

In this issue, Estrada et al. (2003) provide new and important insights into how the endoplasmic reticulum (ER) of budding yeast cells is inherited. Together with other studies in plant and animal cells, the results of Estrada et al. (2003) support the idea that myosin V acts as a universal motor for the transport of ER membranes.
Reproductive Biology and Endocrinology Disruption of the Maxi-k-caveolin-1 Interaction Alters Current Expression in Human Myometrial Cells

Background: One determinant of the total K+ myometrial smooth muscle cell (MSMC) current is the large conductance, calcium-and voltage-activated potassium channel (maxi-K channel). This channel provides a repolarizing current in response to excitatory stimuli, most notably in response to increases in the levels of intracellular Ca2+, and blocking the channel by pharmacological means induces the depolarization of MSMCs and also enhances contraction strength. In MSMCs, maxi-K channels can reside in the caveolae, where they associate with the scaffolding protein caveolin-1 (cav-1). The aim of this study was to investigate the consequences of this interaction-more specifically, how disruption of the association between the maxi-K channel and cav-1 may influence the current expression and excitability of myometrial cells-with the aim of better understanding the mechanisms that underlie the regulation of normal and aberrant uterine function.
Mapping the Substrate of Atrial Fibrillation: Tools and Techniques

Atrial fibrillation (AF) is the most common cardiac arrhythmia that affects an estimated 33.5 million people worldwide. Despite its prevalence and economic burden, treatments remain relatively ineffective. Interventional treatments using catheter ablation have shown more success in cure rates than pharmacologic methods for AF. However, success rates diminish drastically in patients with more advanced forms of the disease. The focus of this research is to develop a mapping strategy to improve the success of ablation. To achieve this goal, I used a computational model of excitation in order to simulate atrial fibrillation and evaluate mapping strategies that could guide ablation. I first propose a substrate guided mapping strategy to allow patient-specific treatment rather than a one size fits all approach. Ablation guided by this method reduced AF episode durations compared to baseline durations and an equal amount of random ablation in computational simulations. Because the accuracy of electrogram mapping is dependent upon catheter-tissue contact, I then provide a method to identify the distance between the electrode recording sites and the tissue surface using only the electrogram signal. The algorithm was validated both in silico and in vivo. Finally, I develop a classification algorithm for the identification of activation patterns using simultaneous, multi-site electrode recordings to aid in the development of an appropriate ablation strategy during AF. These findings provide a framework for future mapping and ablation studies in humans and assist in the development of individualized ablation strategies for patients with higher disease burden.
Diagnosing endocrine hypertension: a practical approach

Hypertension is a leading cardiovascular risk factor that remains difficult to manage in a large segment of the population. Secondary causes of hypertension, which are amenable to targeted treatment or even cure, may contribute to poor blood pressure control. The most common endocrine cause, primary aldosteronism, requires biochemical screening as there are often no symptoms or signs other than hypertension. Screening tests should be performed after adequate preparation to optimize the results and minimize the confounding effects of diet and medications. Further testing beyond the initial screen generally requires input from specialist units to coordinate confirmatory tests and radiological procedures. Other less common or even rare endocrine causes of hypertension generally present with symptoms and signs of pituitary, adrenal, thyroid or parathyroid dysfunction rather than hypertension per se. Here, we review the endocrine causes of hypertension and provide a practical approach to their diagnosis.
Secure quantum signatures using insecure quantum channels

This work was supported by the UK Engineering and Physical Sciences Research Council (EPSRC) under EP/G009821/1 and EP/K022717/1. P.W. gratefully acknowledges support from the COST Action MP1006. A.K. was partially supported by a grant from FQXi and by Perimeter Institute for Theoretical Physics. Research at Perimeter Institute is supported by the Government of Canada through Industry Canada and by the Province of Ontario through the Ministry of Research and Innovation.
Canine renal failure syndrome in three dogs

Three dead dogs were brought to the College of Veterinary Medicine, Kyungpook National University for study. Clinically, all the dogs showed emaciation, anorexia, depression, hemorrhagic vomiting and diarrhea for 7~10 days before death. All the clinical signs were first noted for about one month after feeding the dogs with commercial diets. At necropsy, all 3 dogs had severe renal damage with the same green-yellowish colored nephroliths in the renal pelvis. They also showed systemic hemorrhage and calcification of several organs, which might have been induced by uremia. Microscopically, necrosis, calcification and calculi were detected in the renal tubules, and especially in the proximal convoluted tubules and collecting ducts of the kidney. These findings were supportive of a mycotoxic effect, and especially on their kidneys. However, the precise cause of the toxic effect in these cases of canine renal failure could not be determined.