Objective To evaluate the effect of penehyclidine hydrochloride on hyperoxia-induced acute lung injury and the relationship with endoplasmic reticulum stress-dependent apoptosis in infantile rats.Methods Ninety-six clean-grade male infantile Sprague-Dawley rats,weighing 40-50 g,aged 14 days,were allocated into 4 groups (n =24 each) using a random number table method:control group (C group),penehyclidine hydrochloride group (P group),hyperoxia group (HO group) and hyperoxia plus penehyclidine hydrochloride group (HP group).Infantile rats were intravenously injected with penehyclidine hydrochloride (0.3 mg/kg) at the same time point every day for 3 consecutive days in P and HP groups.Infantile rats were injected with the equal volume of normal saline instead of penehyclidine hydrochloride in C and H groups.Acute lung injury was induced by inhaling oxygen at concentration greater than 90％ for 72 h starting from 4th day after administration.Infantile rats were sacrificed at the end of inhaling,and lungs were removed for examination of the pathological changes and for determination of weight to dry weight ratio (W/D ratio),index of quantitative evaluation for alveolar damage (IQA),pneumonocyte apoptosis (using TUNEL),expression of glucose-regulated protein 78 (GRP78) and CCAAT/enhancer-binding protein homologous protein (CHOP) protein and mRNA in lung tissues (by Western blot or using reverse transcription-polymerase chain reaction).The mitochondrial injury score was assessed,and apoptotic index (AI) was determined.Results Compared with C group,the W/D ratio,IQA,AI and mitochondrial injury score were significantly increased,and the expression of GRP78 and CHOP protein and mRNA was up-regulated in HO and HP groups (P＜0.05),and no significant change was found in the parameters mentioned above in group P (P＞0.05).Compared with HO group,the W/D ratio,IQA,AI and mitochondrial injury score were significantly decreased,the expression of GRP78 and CHOP protein and mRNA was downregulated (P ＜ 0.05),and the pathological changes of lung tissues were significantly attenuated in HP group.Conclusion Penehyclidine hydrochloride can mitigate hyperoxia-induced acute lung injury,and the mechanism may be related to inhibiting endoplasmic reticulum stress-dependent apoptosis in infantile rats.

Objective To study the effect of short-term treatment of subthalamic nucleus ( STN ) deep brain stimulation (DBS) on cerebral glucose metabolism in patients with Parkinson's disease (PD) and its relationship with the change of brain motor-related nerve pathways. Methods Five patients ( 2 males, 3 females;age:(63.6±11.8) years) with PD who underwent STN DBS between January 2014 and December 2018 were enrolled in this study. All patients underwent 18F-fluorodeoxyglucose (FDG) PET in "DBS-off"state before and 3 months after operation. Quantitative expression of PD-related metabolic pattern (PDRP) were calculated by scaled subprofile model/principal component analysis ( SSM/PCA) on PET images. Brain regions with changes of glucose metabolism after DBS were located by statistical parametric mapping (SPM) paired t test. Results Compared with pre-operation, PDRP expression (5.1±1.3 vs 2.9±1.8) and unified Parkinson's disease rating scale (UPDRS) motor score (50.2±8.2 vs 28.0±5.4) of PD patients were significantly decreased 3 months after STN DBS (t values:6.17 and 3.88, both P<0.05). After DBS, the glucose metabolism of bilateral globus pallidus/putamen, caudate nucleus, thalamus, insula, pons and cer-ebellum decreased, while the glucose metabolism of bilateral prefrontal motor area and parietooccipital lobe increased ( t=3.75, P<0.01) . Conclusions Short-term STN DBS therapy can inhibit the cortico-striatum-pallidum-hypothalamus-cortex motor loop, which is abnormally excitable in the brain of PD. PDRP, as an imaging characterization of the regulation of this loop, is expected to become an imaging marker for monito-ring the treatment of PD.

Objective:To investigate characteristics and differences of cerebral glucose metabolism in patients with anti- N-methyl- D-aspartate receptor (NMDAR) encephalitis from the perspective of different trigger factors of antibodies. Methods:A total of 15 patients (8 males, 7 females, age (30.5±17.7) years) with anti-NMDAR encephalitis between January 2016 and January 2019 in Huashan Hospital, Fudan University were recruited retrospectively. All patients underwent resting state cerebral 18F-FDG PET imaging. The characteristics of brain glucose metabolism were analyzed, and the SUV ratio (SUVR) was semi-quantitatively compared with that in 12 healthy subjects (HS; 7 males, 5 females, age (51.5±9.6) years). Independent-sample t test was used to analyze the data. Results:Among 15 patients, 5 patients were viral encephalitis-related anti-NMDAR encephalitis, showing focal decreased metabolism in unilateral temporal lobe or basal ganglia (SUVR: patients: 0.659±0.219; HS: 1.754±0.203; t=-9.58, P<0.001), with increased metabolism in contralateral temporal lobe or basal ganglia (SUVR: patients: 2.275±0.244; HS: 1.960±0.227; t=2.55, P=0.022) in 18F-FDG PET imaging. Six patients were cryptogenic anti-NMDAR encephalitis, showing asymmetric increased metabolism in frontal, temporal, parietal and basal ganglia (SUVR: patients: 2.482±0.395; HS: 1.754±0.203; t=5.23, P<0.001), with decreased metabolism in bilateral occipital lobes. The remaining 4 cases were paraneoplastic origin accompanied by teratoma, showing increased metabolism in bilateral temporal and basal ganglia (SUVR: patient: 2.359±0.181; HS: 1.960±0.227; t=3.16, P=0.007), with mild decreased metabolism in bilateral occipital lobe. Conclusions:The abnormal changes of cerebral glucose metabolism in patients with anti-NMDAR encephalitis can be divided into at least three patterns according to different trigger factors. A comprehensive understanding of these characteristic metabolic changes is helpful for detecting disease, and may provide potential value in indicating different causes.

Purpose To investigate the characteristics of 18F-Florbetaben(18F-FBB)β-amyloid(Aβ)PET imaging in different brain regions of Alzheimer's disease(AD)patients with different degrees of cognitive impairment,and to explore the correlation between Aβ deposition and cognitive dysfunction.Materials and Methods A total of eighteen patients with a clinical diagnosis of probable AD from August 2022 to October 2023 were retrospectively included in Huashan Hospital.All patients had Aβ abnormal deposition in the brain as confirmed by 18F-FBB PET imaging.According to the severity of symptoms,they were divided into the AD-induced mild cognitive impairment(MCI)group(8 cases)and the dementia group(10 cases).In addition,12 healthy controls were included.First,the standardized uptake value ratio of abnormal Aβ deposition in the frontal lobe,lateral parietal lobe,lateral temporal lobe,anterior and posterior cingulate gyrus,and compound cortex was semi-quantitatively calculated and compared among the three groups based on the subjects'brain MRI and automated anatomical labeling template.The correlation between the degree of Aβ deposition in the brains of AD patients and cognitive scale scores(mini-mental state examination,Montreal cognitive assessment)was then further analyzed.Results The standardized uptake value ratio values of Aβabnormal deposition in the frontal lobe,lateral temporal lobe,lateral parietal lobe,anterior and posterior cingulate cortex and compound cortex in the AD-induced MCI and dementia groups were significantly higher than those in the healthy controls(t=7.442-9.151,all P＜0.05).However,there was no significant difference in the standardized uptake value ratio values of Aβ abnormal deposition in the above brain regions between the MCI and dementia groups(t=0.312-0.996,all P＞0.05).In addition,there was no significant correlation between the degree of Aβ deposition in the brain and the cognitive scale scores(mini-mental state examination,Montreal cognitive assessment)in the AD-induced MCI and dementia groups(r=-0.049-0.050,all P＞0.05).Conclusion Aβ deposition in the brains of AD-induced MCI and dementia is significantly higher than in the healthy controls.However,Aβ deposition cannot identify AD patients with different degrees of cognitive impairment,reflecting that Aβ deposition has certain limitations in assessing the severity of clinical symptoms of AD.

Objective: To study the effect of short-term treatment of subthalamic nucleus (STN) deep brain stimulation (DBS) on cerebral glucose metabolism in patients with Parkinson′s disease (PD) and its relationship with the change of brain motor-related nerve pathways. Methods: Five patients (2 males, 3 females; age: (63.6±11.8) years) with PD who underwent STN DBS between January 2014 and December 2018 were enrolled in this study. All patients underwent ¹⁸F-fluorodeoxyglucose (FDG) PET in " DBS-off" state before and 3 months after operation. Quantitative expression of PD-related metabolic pattern (PDRP) were calculated by scaled subprofile model/principal component analysis (SSM/PCA) on PET images. Brain regions with changes of glucose metabolism after DBS were located by statistical parametric mapping (SPM) paired t test. Results: Compared with pre-operation, PDRP expression (5.1±1.3 vs 2.9±1.8) and unified Parkinson′s disease rating scale (UPDRS) motor score (50.2±8.2 vs 28.0±5.4) of PD patients were significantly decreased 3 months after STN DBS (t values: 6.17 and 3.88, both P<0.05). After DBS, the glucose metabolism of bilateral globus pallidus/putamen, caudate nucleus, thalamus, insula, pons and cerebellum decreased, while the glucose metabolism of bilateral prefrontal motor area and parietooccipital lobe increased (t=3.75, P<0.01). Conclusions Short-term STN DBS therapy can inhibit the cortico-striatum-pallidum-hypothalamus-cortex motor loop, which is abnormally excitable in the brain of PD. PDRP, as an imaging characterization of the regulation of this loop, is expected to become an imaging marker for monitoring the treatment of PD.