Delusional parasitosis as presenting symptom of occipital lobe cerebrovascular accident

Delusional parasitosis manifests as a fixed, false belief that an individual is infested by living organisms. Primary delusional parasitosis is a psychiatric disorder with the delusion as an isolated manifestation, whereas secondary delusional parasitosis is a delusion occurring secondary to a psychiatric disorder, substance use, or medical illness. A 62-year-old woman with no psychiatric history presented to the Emergency Department with two to three months of “whole body itching” and seeing small insects crawling on her skin and in her hair. Exam of her skin and scalp was notable for no appreciable lesions, rashes, excoriations, or insects. Her neurologic exam was notable for full visual fields, and no localizing deficits. A non-contrast head CT demonstrated a nonspecific heterogeneous low-attenuation lesion within the medial right occipital lobe, and a follow up MRI confirmed a right posterior cerebral artery distribution subacute infarction. She was admitted for two days, and ultimately was discharged on aspirin and atorvastatin for secondary prevention. An emergency physician should remain vigilant in his/her assessment of patients with seemingly psychiatric symptoms, in particular elderly patients with no known psychiatric illnesses. Neuroimaging should be amongst studies considered in the evaluation of elderly patients presenting with new onset psychiatric complaints.     

Grip strength measurement for frailty assessment in patients with vascular disease and associations with comorbidity,cardiac risk,and sarcopenia

Objective

Frailty is associated with adverse events, length of stay, and nonhome discharge after vascular surgery. Frailty measures based on walking-based tests may be impractical or invalid for patients with walking impairment from symptoms or sequelae of vascular disease. We hypothesized that grip strength is associated with frailty, comorbidity, and cardiac risk among patients with vascular disease.

The Hypotonic Environmental Changes Affect Liposomal Formulations for Nose-to-Brain Targeted Drug Delivery

Systemic administration of drugs is ineffective in the treatment of central nervous system disorders because of the blood-brain barrier. Nasal administration has been suggested as an alternative administration route as drugs absorbed in the olfactory epithelium bypass the blood-brain barrier and reach the brain within minutes. However, the nasal mucosa properties (e.g., tonicity, pH) are not constant because of physiological and environmental factors, and this might limit the therapeutic outcome of nanocarrier-based formulations. To shine light on the impact of environmental ionic strength on nanocarrier-based formulations, we have studied how liposomal formulations respond to the change of tonicity of the external environment. Large unilamellar vesicles loaded with 6 different drugs were exposed to different hypotonic environments, creating an osmotic gradient within the inner core and external environment of the liposomes up to 650 mOsm/kg. Both size and polydispersity of liposomes were significantly affected by tonicity changes. Moreover, the release kinetics of hydrophilic and lipophilic drugs were largely enhanced by hypotonic environments. These results clearly demonstrate that the environmental ionic strength has an impact on liposomal formulation stability and drug release kinetics and it should be considered when liposomal formulations for nose-to-brain targeted drug delivery are designed.     

Treat cancers by targeting survivin: Just a dream or future reality?

Since the discovery of survivin (BIRC5) as a cancer-related molecule by Grazia Ambrosini and Dario C. Altieri at 1997, our knowledge related to the function of this molecule has been extended from simple apoptosis inhibition to complicated, interlinked processes that involve interference of mitosis, apoptosis, autophagy, and even DNA repair recently. However, despite the growing amount of knowledge related to survivin in the last ten years, the development of survivin inhibitors or survivin-related molecular therapies is surprisingly and relatively slow as compared to other therapeutic inhibitors for cancer treatment. Here, the molecular functions of survivin and the progress of development of survivin-targeting therapies are discussed in detail. Functional differences between different survivin-specific inhibitors are discussed from both structural and biochemical point of views. This review also reveals different challenges that scientists are currently facing in the development of survivin inhibitors for clinical application. Finally, future directions for the development of survivin-targeted therapies are discussed in this review.     

Chemotherapy and Radiation Versus Chemotherapy Alone for Elderly Patients With N3 Stage IIIB NSCLC

BackgroundStandard treatment for stage III non–small-cell lung cancer (NSCLC) is concurrent chemotherapy and radiation (chemo-RT). However, N3 stage IIIB disease portends a worse prognosis and the tolerability of chemo-RT in patients ≥70 years old is a concern. In this analysis, we evaluate the survival of patients with N3 stage IIIB NSCLC who were treated with chemo-RT or chemotherapy alone with a focus on elderly patients.Patients and MethodsWe retrospectively analyzed patients diagnosed with N3 stage IIIB NSCLC between 2010 and 2013 using the National Cancer Database. We compared overall survival (OS) between patients who underwent chemo-RT versus chemotherapy alone. The Kaplan–Meier method was used for median OS with log rank tests. Multivariable Cox models were used for multivariable and subgroup analyses.ResultsWe included 9769 patients in our analysis, 7770 of whom received chemo-RT and 1999 who received chemotherapy alone. The median OS for patients who received chemo-RT was 16.4 months versus 12.7 months with chemotherapy alone (P < .0001). The median OS for patients ≥70 years old who received chemo-RT was 15.0 months versus 12.4 months with chemotherapy alone (P < .0001). In multivariable analyses, the benefit of chemo-RT was similar regardless of age. Subgroup analyses in patients ≥70 years indicated a benefit of chemo-RT (hazard ratio, <1.0) across all patient and disease strata.ConclusionSurvival was improved in elderly patients who received chemo-RT versus chemotherapy alone for N3 stage IIIB NSCLC. Our findings suggest that age and comorbidities should not preclude clinicians from recommending chemo-RT to these patients.     

Lysophosphatidylcholine enhances I(Ks) currents in cardiac myocytes through activation of G protein, PKC and Rho signaling pathways

Lysophosphatidylcholine (LPC) is a bioactive phospholipid that accumulates rapidly in the ischemic myocardium. In recent years, it has been shown that some of the actions of LPC are mediated through the activation of the membrane G proteins. However, the precise mechanism(s) responsible for the LPC-related intracellular signaling in the regulation of cardiac ion channels are still poorly understood. The present study was undertaken to examine whether LPC regulates the slow component of the delayed rectifier K⁺ current (I_Ks) and, if so, what intracellular signals are important for this process. Isolated guinea pig cardiac myocytes were voltage-clamped using the whole-cell configuration of the patch-clamp method. The bath application of 1-palmitoyl-lysophosphatidylcholine (LPC-16) concentration-dependently (EC₅₀ = 0.7 μM) and reversibly increased I_Ks in atrial cells, but failed to potentiate I_Ks in ventricular myocytes. In contrast, 1-oleoyl-lysophosphatidylcholine (LPC-18:1) only produced a slight I_Ks increase, and 1-caproyl-lysophosphatidylcholine (LPC-6) or the LPC-16 precursor (phosphatidylcholine) had no effect on I_Ks. Pretreatment of atrial cells with an antibody against the N-terminus of the G2A receptor significantly reduced the LPC-16-induced potentiation of I_Ks. The inhibition of heterotrimeric G protein, phospholipase C (PLC) and protein kinase C (PKC) significantly reduced LPC-16-induced enhancement of I_Ks. Moreover, the blockade of Rho and Rho-kinase by specific inhibitors also inhibited the activity of LPC-16. Immunohistochemical studies demonstrated that G2A was densely distributed in the plasma membrane of atrial myocytes. Therefore, the present study suggests that the activation of a G protein (probably Gα_q) by LPC-16 potentiates I_Ks currents through the PLC-PKC and Rho-kinase pathways.