Diffusion-weighted imaging-based radiomics model using automatic machine learning to differentiate cerebral cystic metastases from brain abscesses.

OBJECTIVES: To develop a radiomics model based on diffusion-weighted imaging (DWI) utilizing automated machine learning method to differentiate cerebral cystic metastases from brain abscesses. MATERIALS AND METHODS: A total of 186 patients with cerebral cystic metastases (n = 98) and brain abscesses (n = 88) from two clinical institutions were retrospectively included. The datasets (129 from institution A) were randomly portioned into separate 75% training and 25% internal testing sets. Radiomics features were extracted from DWI images using two subregions of the lesion (cystic core and solid wall). A thorough image preprocessing method was applied to DWI images to ensure the robustness of radiomics features before feature extraction. Then the Tree-based Pipeline Optimization Tool (TPOT) was utilized to search for the best optimized machine learning pipeline, using a fivefold cross-validation in the training set. The external test set (57 from institution B) was used to evaluate the model's performance. RESULTS: Seven distinct TPOT models were optimized to distinguish between cerebral cystic metastases and abscesses either based on different features combination or using wavelet transform. The optimal model demonstrated an AUC of 1.00, an accuracy of 0.97, sensitivity of 1.00, and specificity of 0.93 in the internal test set, based on the combination of cystic core and solid wall radiomics signature using wavelet transform. In the external test set, this model reached 1.00 AUC, 0.96 accuracy, 1.00 sensitivity, and 0.93 specificity. CONCLUSION: The DWI-based radiomics model established by TPOT exhibits a promising predictive capacity in distinguishing cerebral cystic metastases from abscesses.

Synchronous occurrence of gastrointestinal stromal tumor, pancreatic intraductal papillary mucinous neoplasm, and intrahepatic cholangiocarcinoma: Case report.

RATIONALE: Gastrointestinal stromal tumor (GIST) is the most common primary mesenchymal tumors in gastrointestinal tract. Synchronous occurrence of GIST and tumors in other organs is rare. We first report an exceedingly rare case of synchronous occurrence of gastric GIST, pancreatic intraductal papillary mucinous neoplasm (IPMN) and intrahepatic cholangiocarcinoma. PATIENT CONCERNS: A 70-year-old male presented to our hospital because of abdominal pain and dyspepsia. Tumor markers and liver function were abnormal. Abdomen computed tomography showed concurrent tumors in stomach, pancreas, and liver. DIAGNOSIS: Pathology confirmed synchronous occurrence of gastric GIST, pancreatic IPMN and intrahepatic cholangiocarcinoma. INTERVENTIONS: Mass excision, partly gastrectomy, wedge resection of VIII liver segments, and pancreatic-oduodenectomy were performed. OUTCOMES: During the 18-month follow-up, both laboratory tests and computed tomography examination revealed no sign of recurrence or metastasis. Currently, the patient is free of clinical symptoms such as abdominal discomfort, jaundice, and fever. CONCLUSION: As yet, no cases simultaneously with gastric GIST, pancreatic IPMN and intrahepatic cholangiocarcinoma have been described in literatures. This report increases the knowledge to avoid misdiagnosis and delayed therapy for coexistence of the described 3 types of neoplasm.

The Application of MR Spectroscopy and MR Perfusion in Cerebral Syphilitic Gumma: A Case Report.

Cerebral syphilitic gumma is a rare disease and can be misdiagnosed as a common brain tumor when only conventional imaging results are adopted. Differentiating between syphilitic gumma and tumors may be achieved by applying advanced magnetic resonance (MR) techniques, such as MR spectroscopy and MR perfusion. However, the MR perfusion characteristics of cerebral syphilitic gumma have not been reported yet. Here, we report a case of cerebral syphilitic gumma in a 52-year-old woman and discuss the imaging features of conventional MR, MR spectroscopy, and MR perfusion. The results suggest that the application of MR spectroscopy and MR perfusion could provide additional information that contributes to the diagnosis of cerebral syphilitic gumma.

Sleep deprivation inhibits proliferation of adult hippocampal neural progenitor cells by a mechanism involving IL-17 and p38 MAPK.

Sleep deprivation impairs hippocampal neurogenesis, but the underlying mechanisms are inadequately understood. Sleep deprivation is associated with an increased production of pro-inflammatory factors. In this study, we demonstrate that acute rapid eye movement (REM) sleep deprivation in mice for 3 days leads to increased expression of interleukin (IL)-17A, IL-17F and activation of p38 MAPK pathway in the hippocampus, together with suppressed cell proliferation in the dentate gyrus. Similarly, activation of p38 MAPK and suppressed cell proliferation in the dentate gyrus were observed after administration of recombinant IL-17 in mice without sleep deprivation. Pharmacological blockade of the p38 MAPK after sleep deprivation mitigates sleep deprivation-induced ablation of cell proliferation in the dentate gyrus with unaltered expression of IL-17A and IL-17F. In addition, hippocampal neural progenitor cells express IL-17 receptor A (IL-17RA) and IL-17 receptor C (IL-17RC). These findings suggest that acute REM sleep deprivation suppresses proliferation of adult hippocampal neural progenitor cells by a mechanism involving IL-17 and p38 MAPK signaling.

Diagnosis and Treatment of Spinal Syphilitic Gumma: A Case Report.

Neurosyphilis, which is caused by Treponema pallidum, is a rare sexually transmitted disease involving the central nervous system (CNS). Among all the sub-categories, spinal syphilitic gumma is extremely rare. In previous literature, limited cases of spinal syphilitic gumma have been reported, most of which underwent surgery treatment. In this study, we reported a 46-year-old man, who presented with 5-day numbness of bilateral lower limbs, lower back pain, and irregular defecation. Magnetic resonance imaging (MRI) revealed a homogeneous peripheral enhancement and intramedullary nodule at the T7 level with extensive thoracic cord edema. Combining with laboratory examination results, the syphilitic gumma was considered. One month after the administration of penicillin G, the symptoms vanished. Six months later, MRI indicated no intramedullary nodule.

Sleep and Cognitive Abnormalities in Acute Minor Thalamic Infarction.

In order to characterize sleep and the cognitive patterns in patients with acute minor thalamic infarction (AMTI), we enrolled 27 patients with AMTI and 12 matched healthy individuals. Questionnaires about sleep and cognition as well as polysomnography (PSG) were performed on days 14 and 90 post-stroke. Compared to healthy controls, in patients with AMTI, hyposomnia was more prevalent; sleep architecture was disrupted as indicated by decreased sleep efficiency, increased sleep latency, and decreased non-rapid eye movement sleep stages 2 and 3; more sleep-related breathing disorders occurred; and cognitive functions were worse, especially memory. While sleep apnea and long-delay memory recovered to a large extent in the patients, other sleep and cognitive function deficit often persisted. Patients with AMTI are at an increased risk for hyposomnia, sleep structure disturbance, sleep apnea, and memory deficits. Although these abnormalities improved over time, the slow and incomplete improvement suggest that early management should be considered in these patients.

Sleep abnormality in neuromyelitis optica spectrum disorder.

OBJECTIVES: We investigated the sleep structure of patients with neuromyelitis optica spectrum disorder (NMOSD) and the association of abnormalities with brain lesions. METHODS: This was a prospective cross-sectional study. Thirty-three patients with NMOSD and 20 matched healthy individuals were enrolled. Demographic and clinical characteristics of patients were collected. Questionnaires were used to assess quality of sleep, daytime sleepiness, fatigue, and depression. Nocturnal polysomnography was performed. RESULTS: Compared with healthy controls, patients with NMOSD had decreases in sleep efficiency (7%; p = 0.0341), non-REM sleep N3 (12%; p < 0.0001), and arousal index (6; p = 0.0138). REM sleep increased by 4% (p = 0.0423). There were correlations between arousal index and REM% or Epworth Sleepiness Scale (r = -0.0145; p = 0.0386, respectively). Six patients with NMOSD (18%, 5 without infratentorial lesions and 1 with infratentorial lesions) had a hypopnea index >5, and all of those with sleep apnea had predominantly the peripheral type. The periodic leg movement (PLM) index was higher in patients with NMOSD than in healthy controls (20 vs 2, p = 0.0457). Surprisingly, 77% of the patients with PLM manifested infratentorial lesions. CONCLUSIONS: Sleep architecture was markedly disrupted in patients with NMOSD. Surveillance of nocturnal symptoms and adequate symptomatic control are expected to improve the quality of life of patients with NMOSD.

Sleep-related hypoxemia aggravates systematic inflammation in emphysematous rats.

BACKGROUND: Sleep disturbance is common in patients with emphysema. This study aimed to develop a novel model of sleep-related hypoxemia (SRH) in emphysema (SRHIE) with rats, and to explore the inflammatory status of SRHIE in lung, liver, pancreas, carotid artery and whole blood. METHODS: Seventy-five male Wistar rats were assigned to 5 groups with 15 per group according to the exposure conditions. The protocols varied with the degree of hypoxia exposure and severity of pre-existing emphysema caused by cigarette smoke exposure: (1) SRH control (SRHCtrl) group, sham smoke exposure (smoke exposure, exposed to smoke of 15 cigarettes twice everyday, 16 weeks) and SRH exposure (12.5% O2, 3 hours, SRH exposure, divide total hypoxia time (1.5 hours or 3 hours) into 4 periods evenly (22.5 minutes or 45 minutes) and distribute these hypoxia periods evenly into physiological sleep time of rats identified by electroencephalogram, week 9 to week 16); (2) Emphysema control (ECtrl) group, smoke exposure and sham SRH exposure (21% O2, 3 hours); (3) Short SRH in emphysema (SRHShort) group, smoke exposure and short SRH exposure (12.5% O2, 1.5 hours); (4) Mild SRH in emphysema (SRHMild) group, smoke exposure and mild SRH exposure (15% O2, 3 hours); (5) Standard SRH in emphysema (SRHStand) group, smoke exposure and SRH exposure (12.5% O2, 3 hours). ECtrl, SRHShort, SRHMild and SRHStand groups were groups with emphysematous rats. Two days before the end of exposure, 5 rats in each group were randomly selected for arterial blood gas analysis. In the rest 10 rats in each group, we obtained blood samples and bronchoalveolar lavage fluid (BALF) for routine tests. We also obtained tissue blocks of lung, liver, pancreas, and right carotid artery for pathologic scoring and measurements of liver oxidative stress (measuring hepatic oxidative stress enzymes, superoxide dismutase (SOD) activity, catalase (CAT) activity and malondialdehyde (MDA) concentration). RESULTS: Emphysematous groups had higher mean linear intercept (MLI) and mean alveolar number (MAN) values than SRHCtrl group. MLI values in SRHStand group were the highest (all P < 0.05). O2Sat in SRHStand rats when SRH exposure was (83.45 ± 1.76)%. Histological scores of lung, liver, pancreas and right carotid artery were higher in emphysematous groups than SRHCtrl group, and SRHStand group were the highest (all P < 0.05) (SOD and CAT values were lower and MDA values were higher in groups with emphysema than without and in SRHStand group than in ECtrl group (all P < 0.05)). MDA values were the highest in SRHStand group (all P < 0.05). Total cellular score in BALF and White blood cell (WBC) in whole blood were the highest in SRHStand group (all P < 0.05). Lymphocyte ratios were the highest in SRHStand group both in BALF and blood (all P < 0.05). Red blood cell (RBC) and hemoglobin in emphysematous groups were higher than that in SRHCtrl group, and SRHStand group were higher than ECtrl group (all P < 0.05). CONCLUSIONS: With a proper novo model of SRHIE with Wistar rats, we have demonstrated SRH may aggravate the degree of emphysematous changes, polycythemia, oxidative stress and systematic inflammation. SRH and emphysema may have a synergistic action in causing systematic damages, and lymphocyte may be playing a central role in this process. Longer duration and more severe extent of SRHIE exposure also seem to result in more serious systematic damages. The mechanisms of all these concerned processes remain to be studied.

Inflammation status of rabbit carotid artery model endothelium during intermittent hypoxia exposure and its relationship with leptin.

OBJECTIVES: To develop an intermittent hypoxia/reoxygenation (IH/ROX) rabbit carotid artery model and then investigate the inflammation status of rabbit carotid artery endothelium after IH exposure and its relationship with leptin. MATERIALS AND METHODS: After anesthetization, rabbit's right common carotid artery was cleared of surrounding tissue with anatomic microscope, cannulated to its distal part and the proximal part was ligated. Preparations were challenged by changing the PO(2) of the gas mixture equilibrating the perfusate. Alternate perfusing (2 mL/min) of equilibrated perfusate bubbled with normoxia or hypoxia gas mixtures formed IH/ROX cycles in the right carotid common artery, simulating the pattern of hypoxic episodes seen in obstructive sleep apnea (OSA), or continuous perfusing of hypoxia perfusate to form continuous hypoxia (CH) modes. Sixty adult male New Zealand White rabbits (2.5-3.0 kg) were separated into six groups, ten per group. Groups were: A, intermittent normoxia (IN) group, perfused with perfusion equilibrated with 21% O(2) [PO(2) about 141 +/- 2.87 mmHg] for 15 s and 21% O(2) for 1 min 45 s, 60 cycles; B, severe IH group, 5% O(2) [PO(2) about 35.2 +/- 1.27 mmHg] 15 s and 21% O(2) 1 min 45 s, 60 cycles; C, mild IH group, 10% O(2) [PO(2) about 54.3 +/- 3.31 mmHg] 15 s and 21% O(2) 1 min 45 s, 60 cycles; D, severe IH+Lep group, protocol was the same with severe IH group; E, CH group, IN for 1 h 45 min and then 5% O(2) for 15 min; and F, Lep group, the same with IN group. Right common carotid artery parts distal to the cannula were harvested after exposure, and endothelial cell layers were gotten from longitudinal outspread vessels. Nuclear factor kappaB (NFkappaB) DNA binding activities of partial cell layers were measured with electrophoretic mobility shift assay in the IN group, severe IH group, mild IH group, and CH group nuclear extracts. The other part of the cell layers in the IN group, severe IH group, severe IH+Lep group, and Lep group were cultured for 2 h, and during the culture procedure, recombinated human leptin solutions were added to culture dishes of severe IH+Lep group and Lep group (resulted concentration, 10 ng/mL). Enzyme-linked immunosorbent assay was used to analyze medium interleukin-6 (IL-6) concentrations, reverse transcription polymerase chain reaction was used to analyze endothelial cell Ras homology A (RhoA) mRNA expression levels. Statistical analysis was done with SPSS 11.5 software package. RESULTS: NFkappaB DNA binding activities were significantly different between groups (F = 112.428, P < 0.001). This activity in the severe IH group (4.27 +/- 0.64) was higher than that in the mild IH group (2.33 +/- 0.45, P < 0.001), IN group (1.00 +/- 0.26, P < 0.001), and CH group (1.15 +/- 0.36, P < 0.001). RhoA mRNA expression levels were different in groups (F = 26.634, P < 0.001).This level in the severe IH+Lep group (2.54 +/- 0.53) was higher than that in the severe IH group (1.57 +/- 0.44, P = 0.002), IN group (1.00 +/- 0.31, P < 0.001), and Lep group (1.31 +/- 0.30, P < 0.001). IL-6 concentrations were different in groups (F = 79.922, P < 0.001). IL-6 concentration in the severe IH+Lep group (1591.50 +/- 179.57 pg/mL) was higher than that in the severe IH group (1217.20 +/- 320.62 pg/mL, P = 0.036), IN group (325.40 +/- 85.26 pg/mL, P < 0.001), and Lep group (517.40 +/- 183.09 pg/mL, P < 0.001). CONCLUSIONS: IH/ROX activated the inflammation pathway significantly in the endothelium, which was more intensive than CH and intensity-dependent. When exposed to both IH/ROX and leptin, inflammation occurs more dramatically. It means that synergic activating roles were performed by IH/ROX and leptin. This study may have a clinical implication that IH can cause endothelial damage through activated inflammation in OSA patients, and if the OSA patients have obesity at the same time, the endothelial damage or the inflammation would be more significant because of elevated leptin level as a synergic factor.

[Carotid body inflammation and carotid sinus nerve afferent activity after intermittent hypoxia exposure of various frequencies in rabbits].

OBJECTIVE: To explore the inflammatory reactions, endothelin level and carotid sinus nerve (CSN) afferent activity of carotid body (CB) after intermittent hypoxia/reoxygenation (IH/ROX) exposure of various frequencies in rabbits. METHODS: Forty-nine male adult New Zealand white rabbits (2.5-3.0 kg) were separated into 7 groups (n = 7 each). After anesthetization, the right carotid artery and CSN were cleared of surrounding tissues without touching the right CB and the left carotid region. The CSN was unenveloped to partially expose the myelin sheath, and electrodes were placed to the "single" chemoreceptor bundle of the CSN, with CSN afferent activity carefully monitored and recorded. Then the right common carotid artery was exposed, cannulated to distal part and its proximal part was ligated. Preparations were challenged by changing the PO2 of the gas mixture equilibrating the perfusate. Alternatively perfusion (2 ml/min) of equilibrated perfusate bubbled with normoxia or hypoxia gas mixtures formed IH/ROX cycles in right carotid common artery, simulating the pattern of hypoxic episodes seen in obstructive sleep apnea, or with continuously perfusing hypoxia perfusate to form continuous hypoxia (CH) modes. Groups were defined with different frequencies, and groups were: intermittent normoxia group (IN group) (21% O2, 15 s; 21% O2, 1 min 45 s), 10/hr group (5% O2, 15 s; 21% O2, 5 min 45 s), 30/hr group (5% O2, 15 s; 21% O2, 1 min 45 s), 50/hr group (5% O2, 15 s; 21% O2, 57 s), 60/hr group (5% O2, 15 s; 21% O2, 45 s) and 90/hr group (5% O2, 15 s; 21% O2, 25 s). All the above groups were exposed to 60 treatment cycles; continuous hypoxia group (CH group), IN for 1 h 45 min and then 5% O2 for 15 min. After exposure and 30 min of static placing, CSN afferent frequencies (Charge F) were recorded from chemoreceptor bundles, and the right CB was cleared of surrounding tissues and harvested. Interleukin-6 (IL-6), endothelin-1 (ET-1), hypoxia-inducible factor-1 (HIF-1), and vascular endothelial growth factor (VEGF) concentrations of the CB lysate were measured with enzyme linked immuno sorbent assay (ELISA) kits and standardized. Data were analyzed with SPSS 12.0 software package; and after one way analysis of variance (ANOVA) for whole difference, Tamhane's T2 was used for post hoc analysis. RESULTS: IL-6, ET-1 and Charge F increased but then decreased with increasing IH frequencies (F = 25,601.39, 2390.48, 6945.84, all P values < 0.01). IL-6, ET-1 and Charge F levels in 50/hr group were the highest among groups. Charge F levels correlated significantly with IL-6 or ET-1 (with IL-6: r = 0.736, P < 0.01; with ET-1: r = 0.757, P < 0.01, respectively). IL-6, ET-1 and Charge F levels between IN group and CH group were not statistically different (all P values > 0.05). HIF-1 levels elevated gradually (F = 5241.10, P < 0.01) with increasing exposure frequencies, and the CH group had the highest value (all P values < 0.01). VEGF level in CH group was the highest in all groups (all P values < 0.01). CONCLUSIONS: After IH/ROX exposure, afferent activity of CB CSN increases, which significantly correlates with inflammation and vasomotor mechanism of CB. CB inflammation comes not from IH phases but from ROX phases. Increased CB CSN activity results in elevated SNA tension, which plays a key role in the pathogenesis of systemic hypertension. This procedure influenced by IH/ROX frequencies. CH for 15 min causes no definitely damages. However, HIF-1 and VEGF can be considered as members of adaptive pathway during IH/ROX exposure.

[Stereotactic combined amygdala and hippocampus lesions for treatment of medial temporal lobe epilepsy].

OBJECTIVE: To explore the techniques of stereotactic combined amygdalohippocampotomy for management of medial temporal lobe epilepsy (MTLE). METHODS: The Leksell stereotactic frame was used for all cases, and which almost paralleled the long axis of hippocampus. Stereotactic amygdalohippocampotomy was performed in 23 patients with unilateral medial temporal lobe seizures by using magnetic resonance imaging (MRI) localization for target planning, depth electrode for the electroencephalogram (EEG) monitoring and radiofrequency techniques for lesion production. All procedures were completed under local anesthesia. RESULTS: Pre-lesion spikes or polyspike-waves complex were recorded by a depth electrode in the amygdala and hippocampus region in all patients, and the epileptiform discharges disappeared after the amygdalohippocampotomy. The MRI appearance of the lesion areas after 1 - 2 weeks surgical operation showed that mutiple areas of coagulation necrosis corresponding to the lesion sites were surrounded by zones of edema. Twenty-three patients were followed-up to 8 - 32 months with seizure free 43.48% (10/23), and the general efficiency (seizure reduction >or= 50%) was 91.30% (21/23 cases). CONCLUSIONS: Stereotactic combined lesions of unilateral amygdala and hippocampus for minimally invasive treatment of MTLE is safe and effective, and it is worth to spread in clinical application.