Atrial fibrillation in women versus men: etiology, pathophysiology, treatment, and prognosis

Atrial fibrillation (AF) is the most common arrhythmia, and it predominantly occurs older individuals. Its prevalence is expected to rise as the general population ages. Men have a higher incidence of the disease, but since women have longer lifespans, the absolute numbers of patients with AF are similar across genders. There have been observed differences in the manifestation and outcomes of AF between men and women. Atrial fibrillation has been shown to be partially heritable and might be inherited differently by males and females. The distribution of risk factors has been shown to vary by sex: women tend to present at an older age with comorbid diabetes mellitus, hypertension, and valvular heart disease, while men tend to present with comorbid coronary heart disease. Women with atrial fibrillation have reported worse quality of life, longer duration of symptoms, and atypical symptoms not reported by men. The variations in clinical presentation may be explained by baseline cardiac structural and electrical differences. Men tend to have larger heart sizes, including left atria size and left ventricular wall thickness, which increases the risk of AF. Women tend to have more severe atrial fibrosis, which also increases the risk of AF. Cardiac electrophysiological differences may be impacted by sex hormones. Estrogen and testosterone enact opposite effects on cardiac ion concentrations and action potentials, and thus may affect arrhythmogenesis in men and women. The use of hormone replacement due to menopause has been steadily increasing; atrial fibrillation and hormone replacement overlap in a large number of female patients, but little research has been done into the interaction between the change in hormones and atrial fibrillation. The safety and efficacy of the major treatment options for atrial fibrillation have been compared and studied in men, but women have been underrepresented in these trials. Rhythm and rate control have been shown to yield similar morbidity and mortality in men, but rhythm control has led to worse prognosis in women. While rate control overall may be a better strategy for women, different rate control medications have different safety profiles. Digoxin, a rate control drug, increases the risk of breast cancer, but is the treatment most prescribed to women. Women are more likely to be on pharmacotherapy and are less likely to be referred for electrical cardioversion and ablation, even though studies have found that ablation lowers rates of cardiac and all-cause mortality. Women are also less likely than men to be given anticoagulant therapy to mitigate the risk of stroke, despite female sex being an independent risk factor for AF-associated stroke. The differences in treatment likely explain the observed differences in clinical outcomes between the sexes. Atrial fibrillation in women is associated with higher risks of stroke, cardiac events, cardiovascular mortality, and all-cause mortality. Furthering our understanding of atrial fibrillation is vital for improving outcomes in female patients

ACCESSORY BREAST TISSUE IN THE AXILLA IN A PUERPERAL WOMAN- CASE STUDY

Ectopic or accessory breast tissue (EBT) is an uncommon residual tissue that persists from normal embryonic development, found in 2-6% of the female population. EBT may occur anywhere along the embryonic mammary streak, but is most commonly located in the axillary region. EBT can consist of any or all components of the breast and may be functional or non-functional. The development of this tissue is hormone- dependent, similar to normal breast tissue. EBT presents as asymptomatic mass and may prove to be a diagnostic challenge in the absence of areola and nipple. The identification and distinction of EBT from other breast pathologies occurring in the area, both benign and malignant, is essential for proper management. In most of the cases, these lesions are asymptomatic and do not warrant any intervention unless they produce discomfort. In this report, we present a case of an ectopic breast tissue in the left axilla of an 24-year-old Asian Indian primipara patient. The importance of FNAC as diagnostic tool in suspected cases of polymastia without nipple/areola and the conservative approach through regular follow-up for management of proven benign ectopic breast tissue are highlighted

Computing fuzzy rough approximations in large scale information systems

Rough set theory is a popular and powerful machine learning tool. It is especially suitable for dealing with information systems that exhibit inconsistencies, i.e. objects that have the same values for the conditional attributes but a different value for the decision attribute. In line with the emerging granular computing paradigm, rough set theory groups objects together based on the indiscernibility of their attribute values. Fuzzy rough set theory extends rough set theory to data with continuous attributes, and detects degrees of inconsistency in the data. Key to this is turning the indiscernibility relation into a gradual relation, acknowledging that objects can be similar to a certain extent. In very large datasets with millions of objects, computing the gradual indiscernibility relation (or in other words, the soft granules) is very demanding, both in terms of runtime and in terms of memory. It is however required for the computation of the lower and upper approximations of concepts in the fuzzy rough set analysis pipeline. Current non-distributed implementations in R are limited by memory capacity. For example, we found that a state of the art non-distributed implementation in R could not handle 30,000 rows and 10 attributes on a node with 62GB of memory. This is clearly insufficient to scale fuzzy rough set analysis to massive datasets. In this paper we present a parallel and distributed solution based on Message Passing Interface (MPI) to compute fuzzy rough approximations in very large information systems. Our results show that our parallel approach scales with problem size to information systems with millions of objects. To the best of our knowledge, no other parallel and distributed solutions have been proposed so far in the literature for this problem

1-(3,5-Dimethyl­phen­yl)-4,5-dimethyl-2-phenyl-1H-imidazole hemihydrate

In the title compound, C19H20N2·0.5H2O, the imidazole ring is essentially planar [maximum deviation = 0.005 (1) Å]. The imidazole ring makes dihedral angles of 67.46 (10) and 23.10 (11)° with the attached benzene and phenyl rings, respectively. The dihedral angle between the benzene and phenyl rings is 68.22 (10)°. Inter­molecular O—H⋯N and C—H⋯N hydrogen bonds are found in the crystal structure

4,5-Dimethyl-2-phenyl-1-(p-tol­yl)-1H-imidazole

In the title compound, C18H18N2, the imidazole ring is essentially planar [maximum deviation = 0.004 (1) Å] and makes dihedral angles of 68.91 (8) and 20.43 (9)° with the tolyl and phenyl rings, respectively. The dihedral angle between the latter rings is 73.62 (8)°. The crystal packing is stabilized by inter­molecular C—H⋯N hydrogen bonds

Antibacterial activity of Calathea anulque

No abstrac

Steric hindrance in the upper 50 kDa domain of the motor Myo2p leads to cytokinesis defects in fission yeast

Cytokinesis in many eukaryotes requires a contractile actomyosin ring that is placed at the division site. In fission yeast, which is an attractive organism for the study of cytokinesis, actomyosin ring assembly and contraction requires the myosin II heavy chain Myo2p. Although myo2-E1, a temperature-sensitive mutant defective in the upper 50 kDa domain of Myo2p, has been studied extensively, the molecular basis of the cytokinesis defect is not understood. Here, we isolate myo2-E1-Sup2, an intragenic suppressor that contains the original mutation in myo2-E1 (G345R) and a second mutation in the upper 50 kDa domain (Y297C). Unlike myo2-E1-Sup1, a previously characterized myo2-E1 suppressor, myo2-E1-Sup2 reverses actomyosin ring contraction defects in vitro and in vivo. Structural analysis of available myosin motor domain conformations suggests that a steric clash in myo2-E1, which is caused by the replacement of a glycine with a bulky arginine, is relieved in myo2-E1-Sup2 by mutation of a tyrosine to a smaller cysteine. Our work provides insight into the function of the upper 50 kDa domain of Myo2p, informs a molecular basis for the cytokinesis defect in myo2-E1, and may be relevant to the understanding of certain cardiomyopathies

Fecal Lipocalin 2, a Sensitive and Broadly Dynamic Non- Invasive Biomarker for Intestinal Inflammation

Inflammation has classically been defined histopathologically, especially by the presence of immune cell infiltrates. However, more recent studies suggest a role for low-grade inflammation in a variety of disorders ranging from metabolic syndrome to cancer, which is defined by modest elevations in pro-inflammatory gene expression. Consequently, there is a need for cost-effective, non-invasive biomarkers that, ideally, would have the sensitivity to detect low-grade inflammation and have a dynamic range broad enough to reflect classic robust intestinal inflammation. Herein, we report that, for assessment of intestinal inflammation, fecal lipocalin 2 (Lcn-2), measured by ELISA, serves this purpose. Specifically, using a well-characterized mouse model of DSS colitis, we observed that fecal Lcn-2 and intestinal expression of pro-inflammatory cytokines (IL-1b, CXCL1, TNFa) are modestly but significantly induced by very low concentrations of DSS (0.25 and 0.5%), and become markedly elevated at higher concentrations of DSS (1.0 and 4.0%). As expected, careful histopathologic analysis noted only modest immune infiltrates at low DSS concentration and robust colitis at higher DSS concentrations. In accordance, increased levels of the neutrophil product myeloperoxidase (MPO) was only detected in mice given 1.0 and 4.0% DSS. In addition, fecal Lcn-2 marks the severity of spontaneous colitis development in IL-10 deficient mice. Unlike histopathology, MPO, and q-RT-PCR, the assay of fecal Lcn-2 requires only a stool sample, permits measurement over time, and can detect inflammation as early as 1 day following DSS administration. Thus, assay of fecal Lcn-2 by ELISA can function as a non-invasive, sensitive, dynamic, stable and cost-effective means to monitor intestinal inflammation in mice

2-(4-Fluoro­phen­yl)-4,5-dimethyl-1-(4-methyl­phen­yl)-1H-imidazole

In the title mol­ecule, C18H17FN2, the imidazole ring is essentially planar [maximum deviation of 0.005 (1) Å and makes dihedral angles of 72.33 (8) and 18.71 (8)° with the methyl­phenyl and fluoro­phenyl rings, respectively. The dihedral angle between the two benzene rings is 75.05 (7)°. The crystal packing is stabilized by inter­molecular C—H⋯N hydrogen bonds

Secret-Shared Joins with Multiplicity from Aggregation Trees

We present novel protocols to compute SQL-like join operations on secret shared database tables with non-unique join keys. Previous approaches to the problem had the restriction that the join keys of both the input tables must be unique or had quadratic overhead. Our work lifts this restriction, allowing one or both of the secret shared input tables to have an unknown and unbounded number of repeating join keys while achieving efficient $O(n\log n)$ asymptotic communication/computation and $O(\log n)$ rounds of interaction, independent of the multiplicity of the keys. We present two join protocols, \ProtoUni and \ProtoDup. The first, \ProtoUni is optimized for the case where one table has a unique primary key while the second, \ProtoDup is for the more general setting where both tables contain duplicate keys. Both protocols require $O(n \log n)$ time and $O(\log n)$ rounds to join two tables of size $n$. Our framework for computing joins requires an efficient sorting protocol and generic secure computation for circuits. We concretely instantiate our protocols in the honest majority three-party setting. Our join protocols are built around an efficient method to compute structured aggregations over a secret shared input vector \V\in \mathbb{D}^n. If the parties have another secret-shared vector of control bits \B \in \{0, 1\}^n to partition \V into sub-vectors (that semantically relates to the join operations). A structured aggregation computes a secret shared vector \V\u27\in \mathbb{D}^n where every sub-vector (\V_b,...,\V_e) (defined by the control bits) is aggregated as \V_i\u27=\V_b\op...\op \V_i for $i\in \{b,...,e\}$ according to some user-defined operator \op. Critically, the $b,e$ indices that partition the vector are secret. It\u27s trivial to compute aggregations by sequentially processing the input vector and control bits. This would require $O(n)$ rounds and would be very slow due to network latency. We introduce Aggregation Trees as a general technique to compute aggregations in $O(\log n)$ rounds. For our purpose of computing joins, we instantiate \op \in \textsf{\{copy previous value, add\}}, but we believe that this technique is quite powerful and can find applications in other useful settings