Objective To investigate the role ofglutamic acid decarboxylase autoantibody(GAD-Ab)and protein tyrosine phosphatase autoantibody(IA-2A) in postpartum follow-up of gestational diabetes mellitus (GDM).MethodsGAD-Ab,IA-2A,insulin and glucose metabolism index were measured in 82subjects with normal glucose tolerance (control group) and 84 patients with GDM(GDM group) during 24 to 28 weeks in pregnancy,postpartum 6 to 12 weeks and 2 years.GDM group was divided into antibodies positive group (GAD-Ah or IA-2A were positive) with 18 cases and antibodies negative group (GAD-Ab and IA-2A was negative) with 66 cases.Results Homeostasis model insulin resistance index (HOMA-IR) in GDM group was higher than that in control group (3.87 ± 2.17 vs.2.31 ± 0.52,P ＜ 0.05 ).Homeostasis β -cell function index (HBCI) and 30 min net increment of insulin/30 min net increment of glucose ( △ I30/△ G30) in GDM group were lower than those in control group[206.38 ± 138.06 vs.422.43 ± 228.93 and (20.16 ±11.38) mU/mmol vs.(26.54 ±24.30) mU/mmol,P ＜0.05].The numbers who had the family history of diabetes mellitus and the used of insulin for treatment in antibodies positive group were higher than those in antibodies negative group[ 83.3％ (15/18) vs.28.8％ (19/66) and 77.8％ ( 14/18 ) vs.30.3％ (20/66) ],HOMA-IR,△ I30/ △ G30 and HBCI in antibodies positive group were lower than those in antibodies negative group [3.20±0.84 vs.4.02±0.36,(16.81 ±2.91) mU/mmol vs.(21.55± 11.11) mU/mmol and 124.95 ± 5.03 vs.217.43 ± 115.64,P＜ 0.01 ].Fasting plasma glucose (FPG),2 hours postprandial glucose (2hPG)and glycosylated hemoglobin (HbA1c) in antibodies positive group were higher than those in antibodies negative group during postpartum 6 to 12 weeks and 2 years [postpartum 6 to 12 weeks: (8.20 ±3.11)mmol/L vs.(5.39 ±0.76) mmol/L,(15.22 ±7.29) mmol/L vs.(8.15 ± 1.93) mmol/L,(7.26 ± 1.04)％ vs.(5.88 ±0.41)％ ;postpartum 2 years: (8.91 ±2.80) mmol/L vs.(4.93 ±0.66) mmol/L,(15.75 ±7.87)mmol/L vs.(7.85 ± 1.79) mtmol/L,(7.18 ± 1.22)％ vs.(5.64 ± 0.32 )％,P ＜ 0.01].△ I30/ △ G30 and HBCI were significantly decreased in antibodies positive group postpartum 2 years.No change of the above parameters in antibodies negative group was found.The occurrence rate of type 1 diabetes mellitus (T1DM) was 16.7％(3/18) and 33.3％(6/18) postpartum 6 to 12 weeks and 2 years in antibodies positive group,there was no T1DM in antibodies negative group.ConclusionsWomen with GDM are partly associated with T1DM.Requiring insulin therapy during pregnancy and GAD-Ab or IA-2A positive have considerable risk for developing T1DM.It is also an important predictor to GDM after parturition.

Objective　To explore the risk factors for early deterioration in neurological function/progressive neurological deficit in patients with non-disabling ischemic cerebrovascular events （NICE）. Methods　We conducted a retrospective analysis consecutive patient with non-disabling ischemic cerebrovascular events from the Department of Neurology，the First Affiliated Hospital of Xiamen University between January 2016 and December 2019.Patients were divided into progressive group （n=70） and non-progressive group （n=254） and the term progressive were defined as patients had an increase in National Institutes of Health Stroke Scale（NIHSS） score by ≥2 points within 7-day. Patient demographics，clinical and radiological data were recorded and analyzed. Multinomial logistic regression analysis was performed to determine the independent risk factors for early progression in patients with NICE. Results　On univariate analysis，the incidence of diabetes mellitus，stenosis or occlusion in the corresponding artery，acute infection and new onset ischemic stroke were significantly higher in progressive group than in non-progressive group （P<0.05）.The proportion of higher Fazekas scores （PWMH 2～3，PWMH+DWNH 3～6） in progressive group was significantly higher than that in non-progressive group（P<0.05）. Multivariate logistic regression analysis showed that diabetes mellitus （OR=2.355，95%CI 1.220～4.546，P=0.011），stenosis or occlusion in the corresponding artery （OR=2.542，95%CI 1.405～4.600，P=0.002），acute infection（OR=4.513，95%CI 1.699～11.986，P=0.002），new onset ischemic stroke （OR=2.820，95%CI 1.022～7.781，P=0.045），higher Fazekas scores（PWMH+DWNH 3～6，OR=2.061，95%CI 1.119～3.798，P=0.020；PWMH 2～3，OR=2.046，95%CI 1.096～3.817，P=0.024） were independently associated with early progression in patient with NICE. Conclusion　Diabetes mellitus，stenosis or occlusion in the corresponding artery，acute infection，new onset ischemic stroke，higher Fazekas scores （PWMH+DWNH 3～ 6，PWMH 2～3） may increase the risk of early progression in patient with NICE.

Endogenously eliminating the hematoma is a favorable strategy in addressing intracerebral hemorrhage (ICH). This study sought to determine the role of retinoid X receptor-α (RXR-α) in the context of hematoma absorption after ICH. Our results showed that pharmacologically activating RXR-α with bexarotene significantly accelerated hematoma clearance and alleviated neurological dysfunction after ICH. RXR-α was expressed in microglia/macrophages, neurons, and astrocytes. Mechanistically, bexarotene promoted the nuclear translocation of RXR-α and PPAR-γ, as well as reducing neuroinflammation by modulating microglia/macrophage reprograming from the M1 into the M2 phenotype. Furthermore, all the beneficial effects of RXR-α in ICH were reversed by the PPAR-γ inhibitor GW9662. In conclusion, the pharmacological activation of RXR-α confers robust neuroprotection against ICH by accelerating hematoma clearance and repolarizing microglia/macrophages towards the M2 phenotype through PPAR-γ-related mechanisms. Our data support the notion that RXR-α might be a promising therapeutic target for ICH.

Endogenously eliminating the hematoma is a favorable strategy in addressing intracerebral hemorrhage (ICH). This study sought to determine the role of retinoid X receptor-α (RXR-α) in the context of hematoma absorption after ICH. Our results showed that pharmacologically activating RXR-α with bexarotene significantly accelerated hematoma clearance and alleviated neurological dysfunction after ICH. RXR-α was expressed in microglia/macrophages, neurons, and astrocytes. Mechanistically, bexarotene promoted the nuclear translocation of RXR-α and PPAR-γ, as well as reducing neuroinflammation by modulating microglia/macrophage reprograming from the M1 into the M2 phenotype. Furthermore, all the beneficial effects of RXR-α in ICH were reversed by the PPAR-γ inhibitor GW9662. In conclusion, the pharmacological activation of RXR-α confers robust neuroprotection against ICH by accelerating hematoma clearance and repolarizing microglia/macrophages towards the M2 phenotype through PPAR-γ-related mechanisms. Our data support the notion that RXR-α might be a promising therapeutic target for ICH.
Anilides/pharmacology* ; Cerebral Hemorrhage/drug therapy* ; Hematoma/drug therapy* ; Humans ; Macrophages ; Microglia ; Neuroprotection ; PPAR gamma ; Retinoid X Receptor alpha