Neurosteroids play an important role as endogenous neuromodulators that are locally produced in the central nervous system and rapidly change the excitability of neurons and the activation of microglial cells and astrocytes. Here we review the mechanisms of synthesis, metabolism, and actions of neurosteroids in the central nervous system. Neurosteroids are able to play a variety of roles in the central nervous system under physiological conditions by binding to membrane ion channels and receptors such as gamma-aminobutyric acid type A receptors, Nmethyl-D-aspartate receptors, L- and T-type calcium channels, and sigma-1 receptors. In addition, numerous neurological disorders, including persistent neuropathic pain, multiple sclerosis, and seizures, have altered the levels of neurosteroids in the central nervous system. Thus, we review how local synthesis and metabolism of neurosteroids are modulated in the central nervous system and describe the role of neurosteroids under pathological conditions. Furthermore, we discuss whether neurosteroids may play a role as a new therapeutic for the treatment of neurological disorders.

Neurosteroids play an important role as endogenous neuromodulators that are locally produced in the central nervous system and rapidly change the excitability of neurons and the activation of microglial cells and astrocytes. Here we review the mechanisms of synthesis, metabolism, and actions of neurosteroids in the central nervous system. Neurosteroids are able to play a variety of roles in the central nervous system under physiological conditions by binding to membrane ion channels and receptors such as gamma-aminobutyric acid type A receptors, Nmethyl-D-aspartate receptors, L- and T-type calcium channels, and sigma-1 receptors. In addition, numerous neurological disorders, including persistent neuropathic pain, multiple sclerosis, and seizures, have altered the levels of neurosteroids in the central nervous system. Thus, we review how local synthesis and metabolism of neurosteroids are modulated in the central nervous system and describe the role of neurosteroids under pathological conditions. Furthermore, we discuss whether neurosteroids may play a role as a new therapeutic for the treatment of neurological disorders.

Neurosteroids play an important role as endogenous neuromodulators that are locally produced in the central nervous system and rapidly change the excitability of neurons and the activation of microglial cells and astrocytes. Here we review the mechanisms of synthesis, metabolism, and actions of neurosteroids in the central nervous system. Neurosteroids are able to play a variety of roles in the central nervous system under physiological conditions by binding to membrane ion channels and receptors such as gamma-aminobutyric acid type A receptors, Nmethyl-D-aspartate receptors, L- and T-type calcium channels, and sigma-1 receptors. In addition, numerous neurological disorders, including persistent neuropathic pain, multiple sclerosis, and seizures, have altered the levels of neurosteroids in the central nervous system. Thus, we review how local synthesis and metabolism of neurosteroids are modulated in the central nervous system and describe the role of neurosteroids under pathological conditions. Furthermore, we discuss whether neurosteroids may play a role as a new therapeutic for the treatment of neurological disorders.

Neurosteroids play an important role as endogenous neuromodulators that are locally produced in the central nervous system and rapidly change the excitability of neurons and the activation of microglial cells and astrocytes. Here we review the mechanisms of synthesis, metabolism, and actions of neurosteroids in the central nervous system. Neurosteroids are able to play a variety of roles in the central nervous system under physiological conditions by binding to membrane ion channels and receptors such as gamma-aminobutyric acid type A receptors, Nmethyl-D-aspartate receptors, L- and T-type calcium channels, and sigma-1 receptors. In addition, numerous neurological disorders, including persistent neuropathic pain, multiple sclerosis, and seizures, have altered the levels of neurosteroids in the central nervous system. Thus, we review how local synthesis and metabolism of neurosteroids are modulated in the central nervous system and describe the role of neurosteroids under pathological conditions. Furthermore, we discuss whether neurosteroids may play a role as a new therapeutic for the treatment of neurological disorders.

Neurosteroids play an important role as endogenous neuromodulators that are locally produced in the central nervous system and rapidly change the excitability of neurons and the activation of microglial cells and astrocytes. Here we review the mechanisms of synthesis, metabolism, and actions of neurosteroids in the central nervous system. Neurosteroids are able to play a variety of roles in the central nervous system under physiological conditions by binding to membrane ion channels and receptors such as gamma-aminobutyric acid type A receptors, Nmethyl-D-aspartate receptors, L- and T-type calcium channels, and sigma-1 receptors. In addition, numerous neurological disorders, including persistent neuropathic pain, multiple sclerosis, and seizures, have altered the levels of neurosteroids in the central nervous system. Thus, we review how local synthesis and metabolism of neurosteroids are modulated in the central nervous system and describe the role of neurosteroids under pathological conditions. Furthermore, we discuss whether neurosteroids may play a role as a new therapeutic for the treatment of neurological disorders.

The apocrine morphology of the breast is observed in a broad pathological spectrum, ranging from benign cysts to invasive carcinomas. However, the number of clinical research investigating malignant apocrine lesions is limited. This study retrospectively reviewed the data of patients with malignant apocrine lesions admitted in a tertiary center between January 2004 and December 2021, based on the radiology-pathology correlation and the recent advances in their status to enhance the therapeutic implications of androgen receptor (AR). Among the 37 patients with lesions, 27 (73.0%) had triple-negative subtypes with predominant AR expression. The radiological features of malignant apocrine lesions did not differ from those of typical invasive ductal carcinoma or ductal carcinoma in situ. This study demonstrated that knowledge on the imaging features of malignant apocrine lesions and their histological basis could enhance the adoption of new targeted therapies in patients with this particular type of breast cancer.

Background/Aims: Vascular disease is an established risk factor for stroke in patients with atrial fibrillation (AF), which is included in CHA2DS2-VASc score. However, the role of carotid atherosclerosis remains to be determined. Methods: Three hundred-ten patients with AF who underwent carotid sonography were enrolled. Results: During a median follow-up of 31 months, 18 events (5.8%) of stroke were identified. Patients with stroke had higher carotid intima-media thickness (CIMT) (1.16 ± 0.33 mm vs. 0.98 ± 0.25 mm, p = 0.017). CIMT was significantly increased according to the CHA2DS2-VASc score (p < 0.001) and it was correlated with left ventricular mass index and early diastolic mitral annular velocity (e’), a ratio of early transmitral flow velocity to e’ (E/e’) and pulmonary artery systolic pressure (all p < 0.05). Cox regression using multivariate models showed that carotid plaque was associated with the risk of stroke (hazard ratio, 3.748; 95% confidence interval [CI], 1.107 to 12.688; p = 0.034). C-statistics increased from 0.648 (95% CI, 0.538 to 0.757) to 0.716 (95% CI, 0.628 to 0.804) in the CHA2DS2-VASc score model after the addition of CIMT and carotid plaque as a vascular component (p = 0.013). Conclusions Increased CIMT and presence of carotid plaque are associated with a high risk of ischemic stroke, and CIMT is related to myocardial remodeling and diastolic dysfunction, suggesting that carotid atherosclerosis can improve risk prediction of stroke in patients with AF, when included under vascular disease in the CHA2DS2-VASc scoring system.

Purpose: Nutritional status and support in critically ill patients are important factors in determining patient recovery and prognosis.The aim of this study was to analyze the early nutritional status and the methods of nutritional support in critically ill patients with acute poisoning and to evaluate the effect of nutritional status on prognosis. Methods: A retrospective study was conducted in tertiary care teaching hospital from January 2018 to December 2020. in an emergency department of university hospital, 220 patients who were stayed more than 2 days of poisoning in intensive care unit were enrolled. Results: 155 (70.5%) of patients with acute poisoning had low-risk in nutritional risk screening (NRS). Patients with malignancy had higher NRS (low risk 5.2%, moderate risk 18.5%, high risk 13.2%, p=0.024). Patients of 91.4% supplied nutrition via oral route or enteral route. Parenteral route for starting method of nutritional support were higher in patients with acute poisoning of herbicide or pesticide (medicine 3.2%, herbicide 13.8%, pesticide 22.2%, p=0.000). In multivariate logistic regression analysis, herbicide or pesticide intoxication, higher risk in NRS and sequential organ failure assessment over 4.5 were affecting factor on poor recovery at discharge. Conclusion NRS in patients intoxicated with herbicide or pesticide were higher than that in patients intoxicated with medicine intoxication. Enteral nutrition in patients intoxicated with herbicide or pesticide was less common. Initial NRS was correlated with recovery at discharge in patient with intoxication. It is expected to be helpful in finding patients with high-risk nutritional status in acute poisoning patients and establishing a treatment plan that can actively implement nutritional support.

Objective: To compare short-term treatment outcomes at hospital discharge and hospital length of stay (LOS) in patients with spontaneous intracerebral hemorrhage (sICH) before and after introduction of resident physician work time limit (WTL). Methods: We retrospectively reviewed consecutive patients treated for sICH at our institution between 2016 and 2019. Then we dichotomized these patients into two groups, pre-WTL and post-WTL. We analyzed demographic elements and clinical features, and hospital length of stay (LOS). We evaluated short-term outcome using modified Rankin scale score at hospital discharge and then divided it into “good” and “poor” outcome groups. We subsequently, compared short-term treatment outcome and hospital LOS between the pre-WTL and post-WTL groups. Results: Out of 779 patients, 420 patients (53.9%) were included in the pre-WTL group, and 359 (46.1%) in post-WTL. The mortality rate in sICH patients was higher in the post-WTL group (pre-WTL; 13.6% vs. post-WTL; 17.3%), but there was no statistically significant difference in short-term outcome including mortality (p=0.332) between the groups. The LOS also, was not significantly different between the two groups (pre-WTL; 19.0 days vs. post-WTL; 20.2 days) (p=0.341). The initial Glasgow Coma Scale score, personal stroke history, and mean age were the only independent outcome predicting factors for patients with sICH. Conclusions Some neurosurgeons may expect poorer outcome for sICH after implementation of the WTL of the K-MHW for resident physician however, enforcement of the WTL did not significantly influence the short-term outcome and hospital LOS for sICH in our hospital. Further well-designed multi-institutional prospective studies on the effects of WTL in sICH patient outcome, are anticipated.