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Objective: Mistake in diagnosis Background: Ionizing radiation poses potential health risk to fetuses, including growth retardation, organ malformations, neurological effects, fetal death, and cancer. Therefore, pregnant women rarely undergo X-ray imaging, unless absolutely necessary. However, they can be inadvertently exposed to X-rays while undergoing an examination without being aware of their pregnancy. Given that the likelihood of a fetus appearing on an abdominal radiograph is low, physicians can be unfamiliar with the appearance of a fetus on such images. If a fetus incidentally appears on an abdominal radiograph, the clinician can encounter difficulties in identifying the fetus, potentially leading to unexpected harm during subsequent imaging procedures. Case Report: A 41-year-old woman presented with symptoms of postprandial abdominal pain, abdominal fullness, and urinary frequency. Abdominal radiography revealed a large mass with calcifications in the pelvis and lower abdomen, raising suspicion of a large pelvic tumor, such as a teratoma. However, subsequent ultrasound unexpectedly revealed that the woman was actually 6 months pregnant. The presumed tumor was an enlarged uterus, and the presumed calcifications were the fetus's bones. Before X-ray, the woman had denied being pregnant, mistakenly attributing her condition to excess weight and irregular menstrual cycles. Fortunately, the use of ultrasound instead of computed tomography prevented radiation exposure to the fetus, and the baby was delivered in a healthy state at full term. Conclusions: To avoid unintended harm to fetuses, clinicians should consider the possibility of pregnancy when evaluating a pelvic mass in women of childbearing age. To aid clinicians in accurately identifying fetuses on abdominal radiography and thereby reduce the likelihood of misdiagnosis, we propose the "circled delta sign" and the "reversed circled delta sign". [ABSTRACT FROM AUTHOR]

Excessive maternal high-fructose diet (HFD) during pregnancy and lactation has been reported to cause metabolic disorders in the offspring. Whether the infant’s brain metabolism is disturbed by maternal HFD is largely unknown. Brain energy metabolism is elevated dramatically during fetal and postnatal development, whereby maternal nutrition is a key factor that determines cellular metabolism. Astrocytes, a nonneuronal cell type in the brain, are considered to support the high-energy demands of neurons by supplying lactate. In this study, the effects of maternal HFD on astrocytic glucose metabolism were investigated using hippocampal primary cultures of female infants. We found that glycolytic capacity and mitochondrial respiration and electron transport chain were suppressed by maternal HFD. Mitochondrial DNA copy number and mitochondrial transcription factor A expression were suppressed by maternal HFD. Western blots and immunofluorescent images further indicated that the glucose transporter 1 was downregulated whereas the insulin receptor-α, phospho-insulin receptor substrate-1 (Y612) and the p85 subunit of phosphatidylinositide 3-kinase were upregulated in the HFD group. Pioglitazone, which is known to increase astrocytic glucose metabolism, effectively reversed the suppressed glycolysis, and lactate release was restored. Moreover, pioglitazone also normalized oxidative phosphorylation with an increase of cytosolic ATP. Together, these results suggest that maternal HFD impairs astrocytic energy metabolic pathways that were reversed by pioglitazone. [ABSTRACT FROM AUTHOR]

A 54-year-old man presented with change in behaviour, nocturnal enuresis, abnormal limb movement and headache of one week's duration. The diagnosis of butterfly glioma (glioblastoma multiforme) was made based on imaging characteristics and was further confirmed by biopsy findings. As the corpus callosum is usually resistant to infiltration by tumours, a mass that involves and crosses the corpus callosum is suggestive of an aggressive neoplasm. Other neoplastic and non-neoplastic conditions that may involve the corpus callosum and mimic a butterfly glioma, as well as associated imaging features, are discussed. [ABSTRACT FROM AUTHOR]

Background: Neuroinflammation with activation of microglia and production of proinflammatory cytokines in the brain plays an active role in epileptic disorders. Brain oxidative stress has also been implicated in the pathogenesis of epilepsy. Damage in the hippocampus is associated with temporal lobe epilepsy, a common form of epilepsy in human. Peripheral inflammation may exacerbate neuroinflammation and brain oxidative stress. This study examined the impact of peripheral inflammation on seizure susceptibility and the involvement of neuroinflammation and oxidative stress in the hippocampus. Results: In male, adult Sprague-Dawley rats, peripheral inflammation was induced by the infusion of Escherichia coli lipopolysaccharide (LPS, 2.5 mg/kg/day) into the peritoneal cavity for 7 days via an osmotic minipump. Pharmacological agents were delivered via intracerebroventricular (i.c.v.) infusion with an osmotic minipump. The level of cytokine in plasma or hippocampus was analyzed by ELISA. Redox-related protein expression in hippocampus was evaluated by Western blot. Seizure susceptibility was tested by intraperitoneal (i.p.) injection of kainic acid (KA, 10 mg/kg). We found that i.p. infusion of LPS for 7 days induced peripheral inflammation characterized by the increases in plasma levels of interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). This is associated with a significant increase in number of the activated microglia (Iba-1+cells), enhanced production of proinflammatory cytokines (including IL-1β, IL-6 and TNF-α), and tissue oxidative stress (upregulations of the NADPH oxidase subunits) in the hippocampus. These cellular and molecular responses to peripheral inflammation were notably blunted by i.c.v. infusion of a cycloxygenase-2 inhibitor, NS398 (5 µg/µl/h). The i.c.v. infusion of tempol (2.5 µg/µl/h), a reactive oxygen species scavenger, protected the hippocampus from oxidative damage with no apparent effect on microglia activation or cytokine production after peripheral inflammation. In the KA-induced seizure model, i.c.v. infusion of both NS398 and tempol ameliorated the increase in seizure susceptibility in animals succumbed to the LPS-induced peripheral inflammation. Conclusions: Together these results indicated that LPS-induced peripheral inflammation evoked neuroinflammation and the subsequent oxidative stress in the hippocampus, resulting in the increase in KA-induced seizure susceptibility. Moreover, protection from neuroinflammation and oxidative stress in the hippocampus exerted beneficial effect on seizure susceptibility following peripheral inflammation. [ABSTRACT FROM AUTHOR]

Objectives: To validate next-generation sequencing (NGS) technology for clinical diagnosis and to determine appropriate read depth. Methods: We validated the KRAS, BRAF, and EGFR genes within the Ion AmpliSeq Cancer Hotspot Panel using the Ion Torrent Personal Genome Machine (Life Technologies, Carlsbad, CA). Results: We developed a statistical model to determine the read depth needed for a given percent tumor cellularity and number of functional genomes. Bottlenecking can result from too few input genomes. By using 16 formalin-fixed, paraffin-embedded (FFPE) cancer-free specimens and 118 cancer specimens with known mutation status, we validated the six traditional analytic performance characteristics recommended by the Next-Generation Sequencing: Standardization of Clinical Testing Working Group. Baseline noise is consistent with spontaneous and FFPE-induced C:G→T:A deamination mutations. Conclusions: Redundant bioinformatic pipelines are essential, since a single analysis pipeline gave false-negative and false-positive results. NGS is sufficiently robust for the clinical detection of gene mutations, with attention to potential artifacts. [ABSTRACT FROM AUTHOR]

Quantum decoherence is the loss of a system's purity due to its interaction with the surrounding environment. Via the AdS/CFT correspondence, we study how a system decoheres when its environment is a strongly-coupled theory. In the Feynman- Vernon formalism, we compute the influence functional holographically by relating it to the generating function of Schwinger-Keldysh propagators and thereby obtain the dynamics of the system's density matrix. We present two exactly solvable examples: (1) a straight string in a BTZ black hole and (2) a scalar probe in AdS5. We prepare an initial state that mimics Schrodinger's cat and identify different stages of its decoherence process using the time-scaling behaviors of R'enyi entropy. We also relate decoherence to local quantum quenches, and by comparing the time evolution behaviors of the Wigner function and R'enyi entropy we demonstrate that the relaxation of local quantum excitations leads to the collapse of its wave-function. [ABSTRACT FROM AUTHOR]

Motivated by the recent Kitaev's K-theory analysis of topological insulators and superconductors, we adopt the same framework to study the topological phase structure of Jackiw-Rebbi model in 3+1 dimensions. According to the K-theory analysis based on the properties of the charge conjugation and time reversal symmetries, we classify the topological phases of the model. In particular, we find that there exist Z Majorana zeromodes hosted by the hedgehogs/t'Hooft-Polyakov monopoles, if the model has a T² = 1 time reversal symmetry. Guided by the K-theory results, we then explicitly show that a single Majorana zero mode solution exists for the SU(2) doublet fermions in some codimensional one planes of the mass parameter space. It turns out we can see the existence of none or a single zero mode when the fermion doublet is only two. We then take a step further to consider four-fermion case and find there can be zero, one or two normalizable zero mode in some particular choices of mass matrices. Our results also indicate that a single normalizable Majorana zero mode can be compatible with the cancellation of SU(2) Witten anomaly. [ABSTRACT FROM AUTHOR]

Conjunctival melanoma is an uncommon malignancy with the potential for significant morbidity. Ulceration is known to be an indicator of more aggressive cutaneous melanoma. This factor has not been previously evaluated in conjunctival melanoma. Twenty-six patients with conjunctival melanoma who underwent excision by a single surgeon at a cancer referral center treated between June 2003 and July 2008 were included. The medical records were reviewed for clinical and pathological data. Outcomes assessed included local recurrence, regional lymph node metastasis, distant metastasis, use of adjuvant topical chemotherapy or adjuvant radiation therapy, final visual acuity and death. Local recurrence was seen in three patients (12%). Regional lymph node metastasis and distant metastasis were each seen in four patients (15%). Tumors >2.0 mm thick were more likely to develop distant metastasis than those with a thickness of <2.0 mm (p = 0.0331). Ulceration was noted in 10 of 26 patients. Regional lymph node metastasis and distant metastasis were each seen in 4 of 10 patients with ulceration, and none of the patients without ulceration. Ulceration in conjunctival melanoma may be an important histopathologic predictor of a more aggressive tumor. Globe-sparing multi-modality management of conjunctival melanoma can yield acceptable rates of local-regional recurrence. Savar A, Esmaeli B, Ho H, Liu S, Prieto VG. Conjunctival melanoma: local-regional control rates, and impact of high-risk histopathologic features. [ABSTRACT FROM AUTHOR]

The article presents a case study of a 27-year-old man with a two-month history of floaters, photophobia, and blurry vision of the right eye. He denied any systemic disease and best corrected visual acuity was 20/50 in the right eye and 20/25 in the left eye. The retinal arteries were narrowed and invisible at the far peripheral retina. The article discusses symptomatic sarcoidosis with corticosteroid therapy, and cytotoxic drugs including methotrexate.

We investigate the decoherence patterns of topological qubits in contact with the environment using a novel way of deriving the open system dynamics, rather than using the Feynman–Vernon approach. Each topological qubit is made up of two Majorana modes of a 1D Kitaev chain. These two Majorana modes interact with the environment in an incoherent way which yields peculiar decoherence patterns of the topological qubit. More specifically, we consider the open system dynamics of topological qubits which are weakly coupled to fermionic/bosonic Ohmic-like environments. We find atypical patterns of quantum decoherence. In contrast to the case for non-topological qubits—which always decohere completely in all Ohmic-like environments—topological qubits decohere completely in Ohmic and sub-Ohmic environments but not in super-Ohmic ones. Moreover, we find that the fermion parities of the topological qubits, though they cannot prevent the qubit states from exhibiting decoherence in sub-Ohmic environments, can prevent thermalization turning the state into a Gibbs state. We also study the cases in which each Majorana mode can couple to different Ohmic-like environments, and the time dependence of concurrence for two topological qubits. [ABSTRACT FROM AUTHOR]