Imaging characteristics and prognostic factors of Behcet's disease with arterial involvement: A long-term follow-up study.

PURPOSE: To investigate the imaging characteristics and prognostic factors for the long-term survival of Behcet's disease (BD) with arterial involvement. METHODS: In this retrospective study, BD patients with arterial involvement were identified from January 2003 to January 2020. Arterial lesions were detected by ultrasonography, traditional arteriography, and/or computed tomography angiography (CTA). Cox proportional hazards regression analyses were performed to identify the prognostic factors. RESULTS: Totally, 84 BD patients with arterial involvement were identified (73.8 % males). The mean age at BD diagnosis was 39.1 ± 13.1 years. Arterial involvement was the initial manifestation in 33.3 % of the patients, and the median time from BD diagnosis to arterial involvement was 6 (IQR 1-15.5) years for the rest of patients. Systemic artery involvement and pulmonary artery involvement (PAI) were found in 64 and 27 patients, respectively. Approximately 94.0 % (79/84) of the patients had more than one artery involved concurrently or successively during the course of BD. Aneurysm/dilation was the most prevalent lesion in the aorta (76.0 %), while stenosis/occlusion was the main lesion of the coronary artery (90.9 %) and other aortic branches (74.5 %). Pulmonary hypertension was found in 70.4 % (19/27) of patients with PAI. The 5- and 10-year survival rates of BD patients with arterial involvement were 87.4 % and 84.1 %, respectively. Cardiac involvement (HR: 4.34) and pulmonary artery aneurysm/dilation (HR: 4.89) were independently associated with mortality. CONCLUSIONS: Arterial lesions associated with BD usually involve multiple arteries and manifest differently in different types of arteries. Cardiac involvement and pulmonary artery aneurysm/dilation are independent prognostic factors of BD patients with arterial involvement.

De Winter syndrome and ST-segment elevation myocardial infarction can evolve into one another: Report of two cases.

BACKGROUND: The de Winter electrocardiography (ECG) pattern is a sign that implies proximal left anterior descending coronary artery occlusion in patients with chest pain. The previous view was that the de Winter ECG pattern is static. CASE SUMMARY: A 65-year-old man presented with sudden chest pain at rest associated with diaphoresis for 55 min. The first ECG showed only T-wave inversion in III and aVF leads. Another ECG was performed at the 100th minute, showing upsloping ST segments depressed with tall and symmetrical T waves in the precordial leads; the J point was raised by 0.1 mV at the aVR lead. The patient was referred to our catheterization laboratory. A third ECG showed ST segment elevation by 0.2 mV in the I and aVL leads. The patient underwent emergency coronary angiography, which revealed complete proximal left anterior descending coronary (LAD) occlusion. The second patient presented with a 1-h history of sudden-onset, severe, substernal crushing chest pain. The first ECG showed ST-segment elevation (0.1-1.7 mV) in I, aVL, and precordial leads. The patient was referred to the catheterization laboratory. On arrival, his symptoms alleviated, and ECG showed that the ST-segments had significantly fallen back. The third ECG showed a typical de Winter pattern. Coronary angiography revealed 99% stenosis of the middle LAD. CONCLUSION: The de Winter ECG pattern is transient and dynamic, and it reflects proximal or mid-LAD subtotal occlusion rather than total occlusion.

Autophagy inhibition plays a protective role against 3, 4-methylenedioxymethamphetamine (MDMA)-induced loss of serotonin transporters and depressive-like behaviors in rats.

The 3,4-methylenedioxymethamphetamine (MDMA) is a popular recreational drug, which ultimately leads to serotonergic (5-HT) neurotoxicity and psychiatric disorders. Previous in vitro studies have consistently demonstrated that MDMA provokes autophagic activation, as well as damage of 5-HT axons and nerve fibers. So far, whether autophagy, a well-conserved cellular process that is critical for cell fate, also participates in MDMA-induced neurotoxicity in vivo remains elusive. Here, we first examined time-course of autophagy-related changes during repeated administration of MDMA (10 mg/kg s.c. twice daily for 4 consecutive days) using immunofluorescent staining for tryptophan hydroxylase and microtubule-associated protein 1 light chain 3 beta in rats. We also evaluated the protective effects of 3-methyadanine (3-MA, an autophagy inhibitor, 15 mg/kg i.p.) against MDMA-induced acute and long-term reductions in serotonin transporters (SERT) density in various brain regions using immunohistochemical staining and positron emission tomography (PET) imaging respectively. Plasma corticosterone measurements and forced swim tests were performed to evaluate the depressive performance. The staining results showed that repeated administration of MDMA increased expression of autophagosome and caused reduction in SERT densities of striatum and frontal cortex, which was ameliorated in the presence of 3-MA. PET imaging data also revealed that 3-MA could ameliorate MDMA-induced long-term decreased SERT availability in various brain regions of rats. Furthermore, immobility time of forced swim tests and plasma corticosterone levels were less in the group of MDMA co-injected with 3-MA compared with that of MDMA group. Together, these findings suggest that autophagy inhibition may confer protection against neurobiological and behavioral changes induced by MDMA.

Involvement of autophagy upregulation in 3,4-methylenedioxymethamphetamine ('ecstasy')-induced serotonergic neurotoxicity.

It has been suggested that autophagy plays pathogenetic roles in cerebral ischemia, brain trauma, and neurodegenerative disorders. 3,4-Methylenedioxymethamphetamine (MDMA or ecstasy) is an illicit drug that causes long-term serotonergic neurotoxicity in the brain. Apoptosis and necrosis have been implicated in MDMA-induced neurotoxicity, but the role of autophagy in MDMA-elicited serotonergic toxicity has not been investigated. The present study aimed to examine the contribution of autophagy to neurotoxicity in serotonergic neurons in in vitro and in vivo animal models challenged with MDMA. Here, we demonstrated that in cultured rat serotonergic neurons, MDMA exposure induced LC3B-densely stained autophagosome formation, accompanying by a decrease in neurite outgrowth. Autophagy inhibitor 3-methyladenine (3-MA) significantly attenuated MDMA-induced autophagosome accumulation, and ameliorated MDMA-triggered serotonergic neurite damage and neuron death. In contrast, enhanced autophagy flux by rapamycin or impaired autophagosome clearance by bafilomycin A1 led to more autophagosome accumulation in serotonergic neurons and aggravated neurite degeneration. In addition, MDMA-induced autophagy activation in cultured serotonergic neurons might be mediated by serotonin transporter (SERT). In an in vivo animal model administered MDMA, neuroimaging showed that 3-MA protected the serotonin system against MDMA-induced downregulation of SERT evaluated by animal-PET with 4-[(18)F]-ADAM, a SERT radioligand. Taken together, our results demonstrated that MDMA triggers upregulation of autophagy in serotonergic neurons, which appears to be detrimental to neuronal growth.