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Ferroptosis Mechanisms Involved in Hippocampal-Related Diseases.
BACKGROUND Intracytoplasmic lumina (ICL) are observed in several cancers, including urothelial carcinoma (UC). We have reported that ICL in urine cytology (cICL) is more frequent in high-grade UCs than in low-grade UCs; however, the correlation between the presence of ICL and prognosis is unclear. OBJECTIVES The aim of this work was to determine the association between cICL and prognosis in bladder cancer. METHOD We retrospectively investigated 87 patients with bladder cancer who received a histological diagnosis within 3 months of urine cytology at Kanazawa Medical University between 2003 and 2007. The cytological diagnosis and the number of cICL, histological diagnosis, tumor grade or variant, pT stage, ICL in histological specimens, and immunohistochemistry for mucins were evaluated. Data on the treatment type, recurrence, survival, cause of death, and length of follow-up were collected from electronic medical records. RESULTS Muscle invasion, high-grade UC, lymph node metastasis, distant metastasis, adjuv a worse prognosis in urine cytology. © 2020 S. Karger AG, Basel.BACKGROUND In 2014, the World Health Organization (WHO) released a classification system introducing neuroendocrine neoplasms (NENs) of the female reproductive tract, excluding the ovaries. This study aimed to evaluate whether retrospective adaption of the gastroenteropancreatic (GEP)-NEN classification is feasible for ovarian NENs (O-NENs) and correlates with prognosis. METHODS Sixty-eight patients diagnosed with carcinoid, small cell carcinoma (pulmonary type), paraganglioma, non-small/large cell neuroendocrine carcinoma (NEC), mixed NEC, or undifferentiated carcinomas at 20 institutions in Japan were included in this retrospective cross-sectional study. We identified O-NENs through central pathological review using a common slide set, followed by reclassification according to WHO 2010 guidelines for GEP-NENs. A proportional hazards model was used to assess the association of prognostic factors (age, stage, performance status, histology, and residual disease) with overall survival (OS) and progression-free survival (PFS). RESULTS Of the 68 enrolled patients, 48 were eligible for analysis. All carcinoids (n = 32) were reclassified as NET G1/G2, whereas 14 of 16 carcinomas were reclassified as NEC/mixed adeno-NEC (MANEC) (Fisher's exact test, p less then 0.01). The OS/PFS was 49.0/42.5 months and 6.5/3.9 months for NET G1/G2 and NEC/MANEC, respectively. Histology revealed that NEC/MANEC was associated with increased risk of death (HR = 48.0; 95% CI, 3.93-586; p less then 0.01) and disease progression (HR = 51.6; 95% CI, 5.54-480; p less then 0.01). CONCLUSION Retrospective adaption of GEP-NEN classification to O-NENs is feasible and correlates well with the prognosis of O-NENs. This classification could be introduced for ovarian tumors. UMIN Clinical Trials Registry number UMIN000019754. © 2020 S. Karger AG, Basel.OBJECTIVE Diabetic cardiomyopathy (DCM) is a serious complication of type 2 diabetes mellitus (T2DM), resulting in unfavorable prognosis. Icariin (ICA) is a major flavonoid isolated from the traditional oriental herbal medicine Epimedium that has been recently proved to show potential therapeutic efficacy on T2DM. The aim of this study was to investigate the underlying mechanism of how ICA improved DCM in rat models. METHODS To corroborate myocardial improvement by ICA, we managed to establish the T2DM rat model by streptozotocin (STZ) administration and high-glucose-high-fat diet. RESULTS The rats with T2DM showed severe insulin resistance, left ventricular dysfunction, aberrant lipids deposition, cardiac inflammation, and fibrosis compared with the control group. All these pathological symptoms were ameliorated by the treatment of ICA. The levels of extracellular matrix proteins of heart tissue significantly declined in ICA-treated rats. CONCLUSION ICA may exert as a protector in T2DM-induced DCM by reducing extracellular matrix proteins in the heart tissue, implicating its potential role for the treatment of human DCM. © 2020 S. Karger AG, Basel.A time-dependent loss of cell solute protects against lethal cerebral edema in hyponatremia. This adaptation, which makes survival possible when the serum sodium concentration is extremely low, also makes the brain vulnerable to injury if chronic (>48 hours) hyponatremia is corrected more rapidly than lost brain solutes can be recovered. Rapid correction of chronic hyponatremia results in programmed cell death of astrocytes and oligodendrocytes and presents clinically with a delayed onset of neurological findings, known as the osmotic demyelination syndrome. This iatrogenic complication can be avoided by limiting correction of hyponatremia to less then 8 mEq/L per day. © 2019 S. Clozapine N-oxide Karger AG, Basel.The etiology of hyponatremia is often multifactorial. The most common causes include hypovolemia from gastrointestinal (GI) or other fluid losses, thiazide diuretics, and SIAD []. The management of hypovolemic hyponatremia starts with confirming its presence and determining the underlying cause. Correction focuses on the appropriate use of isotonic fluid to effect volume repletion while avoiding an overly rapid rise in serum [Na+] concentration. © 2019 S. Karger AG, Basel.Hyponatremia is the commonest electrolyte deficiency in clinical practice. Of the many causes of hyponatremia, syndrome of inappropriate antidiuresis (SIAD) is the commonest. Glucocorticoid deficiency, due to central/secondary adrenal insufficiency, is the key differential diagnosis for SIAD, as it presents with a similar biochemical picture of euvolemic hyponatremia and inappropriate urinary concentration. The underlying mechanisms for the development of hyponatremia in glucocorticoid deficiency are (1) impaired renal water handling in the absence of circulating cortisol and (2) increased plasma concentrations of arginine vasopressin (AVP), despite hypo-osmolality. The original diagnostic criteria for SIAD emphasized that normal adrenal reserve was essential for its diagnosis, in recognition of the similar biochemical presentation of SIAD and glucocorticoid deficiency. This has been emphasized in all of the recently published clinical guidelines. However, data from the literature suggest that clinicians ignore the measurement of plasma cortisol concentration in both clinical practice and research protocols.
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