Spontaneous intracranial hypotension in a patient without corpus callosum: A case report.

RATIONALE: Spontaneous intracranial hypotension (SIH) is a well-established condition typically presenting with disabling orthostatic headache. Corpus callosum agenesis (CCA) is one of the most common human brain malformations with a wide spectrum of associated malformations, chromosomal abnormalities, and clinical syndromes. PATIENT CONCERNS: A 53-year-old woman presented with recurrent orthostatic headache for about 1 month. The head computed tomography examination of the patient showed CCA and the initial pressure of subsequent lumbar puncture was only 5 centimeters cerebrospinal fluid. Magnetic resonance imaging examination confirmed CCA with gray matter heterotopia. DIAGNOSIS: The final diagnose was SIH related headache with CCA. INTERVENTION: The patient's symptom improved after oral hydration, intravenous fluids, and bed rest. OUTCOME: Favorable outcome was observed. LESSONS: Although this co-occurrence of SIH and CCA is probably coincidental, this finding suggests that the developmental malformations of the brain may lead to structural changes in brain tissue or disturbances in cerebrospinal fluid production and reflux, resulting in pathological changes over time.

Orientin inhibits inflammation in chondrocytes and attenuates osteoarthritis through Nrf2/NF-κB and SIRT6/NF-κB pathway.

Effects of Orientin on murine chondrocytes treated with interleukin-1ß (IL-1ß) were evaluated using qPCR, western blot analysis, ELISA, and immunofluorescent staining in vitro. In vivo, We established a standard OA model by performing the destabilized medial meniscus (DMM) surgery on C57BL/6 mice, and assessed healing effect of Orientin by X-ray imaging, histopathological analysis, immunohistochemical staining. Osteoarthritis (OA) is the most common form of degenerative joint disease in clinic and the chondrocyte inflammation plays the most important role in OA development. The natural flavonoid compound (Orientin) has anti-inflammatory bioactive properties in the treatment of various diseases. But studies have not explored whether Orientin modulates OA progression. In this study, a significant suppression in IL-1ß-mediated pro-inflammatory mediators and the degradation of cartilage extracellular matrix (ECM) was observed in vitro through qPCR, western blot analysis, ELISA, and immunofluorescent staining after the treatment with Orientin. In addition, Orientin abrogated DMM surgery induced cartilage degradation in mice, which was assessed by X-ray imaging, histopathological analysis, immunohistochemical staining. Mechanistic studies showed that Orientin suppressed OA development by downregulating activation of NF-κB by activating Nrf2/HO-1 axis and SIRT6 signaling pathway. These results provide evidence that Orientin serves as a potentially viable compound for the treatment of OA.

Effect of triadimefon on rat placental morphology, function, and gene expression.

Triadimefon is a fungicide that is broadly used to treat fungal diseases of plants. It causes developmental toxicity in the animal model. Whether triadimefon disrupts the placental function and the underlying mechanism remains unclear. Thirty-six female pregnant Sprague-Dawley rats were randomly assigned into four groups and were orally administered via gavage of triadimefon (0, 25, 50, and 100 mg/kg/day) for 10 days from gestational day (GD) 12-21. Triadimefon disrupted the structure of the placenta, leading to hypertrophy, abnormal hemodynamics, including fibrin exudation, edema, hemorrhage, infarction, and inflammation. RNA-seq analysis showed that triadimefon down-regulated the expression of developmental and metabolic genes, while up-regulating the immune/inflammatory genes. The qPCR showed that triadimefon markedly down-regulated the expression of Cpt1c, Scd2, Ldlr, Dvl1, Flt4, and Vwf and their proteins, while up-regulating the expression of Cyp1a1, Star, Ccl5, and Cx3cr1 and their proteins at 25-100 mg/kg. Western blot showed that triadimefon reduced the level of STAT3 at doses of 50 and 100 mg/kg and the phosphorylation of AMPK at 100 mg/kg. In conclusion, triadimefon severely damages the structure and function of the placenta, leading to placental hypertrophy, local blood circulation disorders, and inflammation and this may be associated with its down-regulation of genes related to metabolism and nutrient transport and the up-regulation of inflammatory genes via STAT3 and AMPK signals.