A detailed biophysical model for a neuron/astrocyte network is developed in order to explore mechanisms responsible for the initiation and propagation of recurrent cortical spreading depolarizations. The model incorporates biophysical processes not considered in the earlier models. This includes a model for the Na-glutamate transporter, which allows for a detailed description of reverse glutamate uptake. In particular, we consider the specific roles of elevated extracellular glutamate and K in the initiation, propagation and recurrence of spreading depolarizations.

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A 56 years old male patient presented to our institution with a gradually progressive bulbous, multi-lobular, non-tender,rm, rubbery swelling of tip and dorsum of nose over last 20 years, extending to bilateral alae, with prominent skin pores, causing functional and cosmetic impairment. Condition was clinically diagnosed as rhinophyma and accorded 6 points under Rhinophyma Severity Scale. Under general anaesthesia, excision was done by shaving of the mass from underlying cartilage without damaging it, with the use of loop electro-cautery. Wound was allowed to granulate and heal by secondary intention, with no recurrence observed in follow-up. Histopathological examination conrmed rhinophyma

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Introduction: Previous studies of the relationship between cerebral small vessel disease (CSVD) lesions and carotid artery (CA) calcifications have yielded conflicting results. Hypothesis: We hypothesized that intracranial ICA (ICICA) calcifications are most closely associated with CSVD in comparison to extracranial ICA (ECICA) and common CA (CCA) calcifications. Methods: Acute ischemic stroke and transient ischemic attack patients were recruited into a hospital-based prospective stroke registry. Total CSVD burden score including white matter hyperintensity (WMH), lacunes, microbleeds (MBs) and enlarged perivascular spaces (PVS) was measured according to Staals et al. Fazekas scale was used to rate the periventricular and deep WMH (PVMH and DWMH respectively). ICICA calcifications were measured on plain head CT scan according to Subedi et al. ECICA and CCA calcifications were measured according to Yamada et al on the neck CT angiography. Univariate analyses were used to test the relationship between CSVD lesions and CA calcifications. Binary and ordered logistic regression analyses were performed to adjust for the effect of age, sex, race, history of hypertension, diabetes and current smoking for the variables that showed significance in the univariate analyses. Results: 141 patients (age 64.5±15.3, 49% females, total CSVD score 1.6±1.4, ICICA, ECICA and CCA calcification scores were 7.8±9.9, 10.3±13.4 and 2.1±6.9, respectively). In Univariate analyses, ICICA calcification score showed significant relationships with PVMH, DWMH, lacunes, MBs and total CSVD scores ( P values: <0.0001, 0.0005, 0.0078, 0.049 and 0.0026 respectively). ECICA calcification score showed significant relationships with PVWMH and DWMH (P values: 0.0062 and 0.0332, respectively) while CC calcification score showed significant relationships with PVMWH, DWMH, MBs and PVS (P values: 0.0008, 0.034, 0.045 and 0.013). Multivariate analyses showed significant relationships only for PVWMH and DWMH with ICICA calcification (P values: 0.008 and 0.05, respectively). Conclusions: ICICA calcifications are most closely linked to PVMW and DWMH. Further studies are required to investigate the pathophysiological mechanisms behind this relationship.