Partially Reversible FLAIR Hyperintensity Along the Brainstem Surface in Autoimmune Glial Fibrillary Acidic Protein Astrocytopathy.

A 41-year-old woman presented with headache, fever, irritability, and confusion. She developed a coma after admission. MRI of the brain revealed periventricular and deep white matter lesions. Fluid-attenuated inversion recovery (FLAIR) and diffusion-weighted imaging hyperintensity along the brainstem surface was observed (Figure 1), considered a rare but characteristic finding in leptomeningeal carcinomatosis from lung cancer.1,2 However, serum tumor markers, CSF cytopathology, contrast-enhanced high-resolution chest CT, and whole-body PET were negative. Antiglial fibrillary acidic protein antibodies (cell-based assay) were positive in serum and CSF. After receiving intravenous methylprednisolone and immunoglobulin, the symptoms improved significantly. Repeated MRI of the brain showed partial resolution of the lesions (Figure 2). The lesions were possibly induced by immune-mediated intramyelinic edema.

Comparison of Characteristics and Outcomes Between Acute Ischemic Stroke Patients with Different Types of Heart Failure.

Acute ischemic stroke (AIS) can be complicated by heart failure involving preserved ejection fraction (HFpEF) or reduced ejection fraction (HFrEF), and whether or not the prognosis differs between the 2 types of patients remains unclear. We compared the clinical characteristics and outcomes of the 2 types of patients at 3 months after the stroke.We retrospectively analyzed patients who, between 1 January 2018 and 1 January 2021, experienced AIS that was complicated by HFrEF or HFpEF. All patients had been prospectively registered in the Chengdu Stroke Registry. Poor outcome was defined as a modified Rankin Scale (mRS) score of 2-6 at 3 months. Univariate and binary logistic regression was used to assess whether HFpEF was associated with a significantly worse prognosis than HFrEF.Among the final sample of 108 patients (60.2% men; mean age, 73.08 ± 10.82 years), 75 (69.4%) had HFpEF. Compared to HFrEF patients, those with HFpEF were older (P = 0.002), were more likely to have chronic kidney disease (P = 0.033), and were more likely to experience a poor outcome (P = 0.022). After adjustments, HFpEF was associated with significantly greater risk of poor outcome than HFrEF (OR 4.13, 95%CI 1.20-15.79, P = 0.029). However, rates of hemorrhagic transformation or mortality at 3 months after AIS did not differ significantly between the 2 types of heart failure (all P > 0.05).Patients with AIS involving HFpEF experience worse outcomes than those with HFrEF and therefore may require special monitoring and management. Our findings need to be verified in large prospective studies.

Acute inferior myocardial infarction combined with papillary muscle rupture: A case report. / 急性下壁心肌梗死合并乳头肌断裂1例.

The incidence of acute myocardial infarction (AMI) is increasing. Acute papillary muscle rupture is one of the serious and rare mechanical complications of AMI, which occurs mostly in inferior and posterior myocardial infarction. A patient with acute inferior myocardial infarction developed pulmonary edema and refractory shock, followed by cardiac arrest. After cardiopulmonary resuscitation (CPR), revascularization of criminal vessels was carried out by emergency percutaneous transluminal coronary angioplasty (PTCA) under the support of intra-aortic balloon pump (IABP) and extra corporeal membrane oxygenation (ECMO). Although the patient was given a chance for surgery, his family gave up treatment due to unsuccessful brain resuscitation. It reminds that mechanical complications such as acute papillary muscle rupture, valvular dysfunction and rupture of the heart should be highly suspected when cardiogenic pulmonary edema and cardiogenic shock are difficult to correct in acute inferior myocardial infarction. Echocardiogram and surgery should be put forward when revascularization of criminal vessels is available.

Clinical, radiological and pathological characteristics of moderate to fulminant psittacosis pneumonia.

BACKGROUND: Psittacosis pneumonia is a community-acquired pneumonia caused by Chlamydia psittaci. It is usually under-diagnosed due to its atypical clinical presentation and lack of routine laboratory tests. METHODS: To better understand the clinical features, 52 patients diagnosed with psittacosis pneumonia by metagenomic next-generation sequencing (mNGS) were enrolled in this study. The clinical, radiological and pathological characteristics were retrospectively analyzed. RESULTS: The onset of psittacosis pneumonia in this study occurred all year round, with a peak from December to January. Most of the patients were 51-80 years old. About 65.38% of patients had a history of exposure to poultry or parrots. Abnormalities of multiple clinical signals were detected in these patients. Elevated levels of neutrophil ratio, C-reactive protein, erythrocyte sedimentation rate, and procalcitonin were detected in most patients. Radiological evidence revealed air-space consolidation or ground-glass opacities in lungs of all patients, which is the typical feature of psittacosis pneumonia. In addition, hyperemia, swelling of bronchial mucosa, and bronchial patency were detected by bronchoscopy in all patients, and bronchial sub-mucosal edema, inflammatory cells infiltration and alveolar epithelial hyperplasia were identified in the bronchial mucosa and alveolar tissue. Beta-lactam antibiotics were administered for empirical treatment before mNGS in 17 patients but showed no improvement. The treatment was switched to doxycycline or moxifloxacin immediately since psittacosis pneumonia were suspected and confirmed by mNGS detection (within 48 hours). After receiving adjustment of treatment, 94.23% (49/52) of patients were cured successfully. CONCLUSIONS: In conclusion, mNGS may be a promising approach for clinical diagnosis of psittacosis. For patients with a history of exposure to birds, hyperpyrexia, nonproductive cough, multiple elevated inflammatory markers, and air-space consolidation in lung, psittacosis pneumonia should be considered, especially when beta-lactam antibiotics showed limited efficacy.

Liver fibrosis indices associated with substantial hematoma expansion in Chinese patients with primary intracerebral hemorrhage.

BACKGROUND: Whether liver fibrosis is associated with increased risk for substantial hematoma expansion (HE) after intracerebral hemorrhage (ICH) is still uncertain. We evaluated the association between various liver fibrosis indices and substantial HE in a Chinese population with primary ICH. METHODS: Primary ICH patients admitted to West China Hospital within 24 h of onset between January 2015 and June 2018 were consecutively enrolled. Six liver fibrosis indices were calculated, including aspartate aminotransferase (AST)-platelet ratio index (APRI), AST/alanine aminotransferase ratio-platelet ratio index (AARPRI), fibrosis-4 (FIB-4), modified fibrosis-4 (mFIB-4), fibrosis quotient (FibroQ) and Forns index. Substantial HE was defined as an increase of more than 33% or 6 mL from baseline ICH volume. The association of each fibrosis index with substantial HE was analyzed using binary logistic regression. RESULTS: Of 436 patients enrolled, about 85% showed largely normal results on standard hepatic assays and coagulation parameters. Substantial HE occurred in 115 (26.4%) patients. After adjustment, AARPRI (OR 1.26, 95% CI 1.00-1.57) and FIB-4 (OR 1.15, 95% CI 1.02-1.30) were independently associated with substantial HE in ICH patients within 24 h of onset, respectively. In ICH patients within 6 h of onset, each of the following indices was independently associated with substantial HE: APRI (OR 2.64, 95% CI 1.30-5,36), AARPRI (OR 1.55, 95% CI 1.09-2.21), FIB-4 (OR 1.35, 95% CI 1.08-1.68), mFIB-4 (OR 1.09, 95% CI 1.01-1.18), FibroQ (OR 1.08, 95% CI 1.00-1.16) and Forns index (OR 1.37, 95% CI 1.10-1.69). CONCLUSIONS: Liver fibrosis indices are independently associated with higher risk of substantial HE in Chinese patients with primary ICH, which suggesting that subclinical liver fibrosis could be routinely assessed in such patients to identify those at high risk of substantial HE.

Serum Albumin as a Potential Predictor of Pneumonia after an Acute Ischemic Stroke.

BACKGROUND: Serum albumin level is associated with infection after stroke, but whether albumin predicts post-stroke pneumonia is unclear. The potential relationship between albumin level and pneumonia in patients with acute ischemic stroke (AIS) was evaluated in this study. METHODS: A consecutive sample of 798 AIS patients who were admitted to West China Hospital within 24 h after onset, from the year 2017 to 2018, were retrospectively analyzed. Blood was collected on admission and assayed for serum albumin. Univariate analyses, multivariate logistic regression, and stratified logistic regression were performed to identify the risk factors of post-stroke pneumonia. RESULTS: Out of the 798 patients, 240 (30.2%) developed pneumonia at a median of 48 h after onset (interquartile range, 27-74 h). Patients with pneumonia had significantly lower serum albumin levels than those without pneumonia (40.6 vs. 42.9 g/l, p<0.001). After adjustment, the albumin level was still significantly associated with pneumonia in multivariate logistic regression (odds ratio [OR] 0.87, 95% confidence interval [CI] 0.81-0.94). The association between serum albumin and pneumonia tended to depend on National Institutes of Health Stroke Scale score (p = 0.045), but this was significant only in patients with mild stroke (OR 0.84, 95% CI 0.77-0.93). A dosedependent inverse relationship was found between albumin levels and the risk of pneumonia after AIS. Albumin values predicted pneumonia with an area under the curve of 0.661 (95% CI 0.620- 0.701), and the optimal cutoff was 42.6 g/L. CONCLUSION: Low serum albumin levels may be independent predictors of pneumonia in patients with AIS, especially in mild stroke. In fact, the risk of pneumonia may vary inversely with albumin level.

Treatment of invasive fungal disease: A case report.

BACKGROUND: In recent years, the incidence of fungal infection has been increasing, often invading one or more systems of the body. However, it is rare for lymph nodes to be invaded without the involvement of other organs. CASE SUMMARY: A 21-year-old man was admitted to hospital for repeated cough for 2 mo and abdominal pain for 1 mo. Physical examination revealed multiple lymph nodes enlargement, especially those in the left neck and groin. CT scan showed multiple lymph nodes enlargement in the chest, especially left lung, abdominal cavity, and retroperitoneum. The first lymph node biopsy revealed granulomatous lesions of lymph nodes, so intravenous infusion of Cefoperazone tazobactam combined with anti-tuberculosis drugs were given. Because fever and respiratory failure occurred 4 d after admission, mechanical ventilation was given, and Caspofungin and Voriconazole were used successively. However, the disease still could not be controlled. On the 11th day of admission, the body temperature reached 40° C. After mycosis of lymph nodes was confirmed by the second lymph node biopsy, Amphotericin B was given, and the patient recovered and was discharged from the hospital. CONCLUSION: No fixed target organ was identified in this case, and only lymph node involvement was found. Caspofungin, a new antifungal drug, and the conventional first choice drug, Voriconazole, were ineffective, while Amphotericin B was effective.

Brain Natriuretic Peptide-Regulated Expression of Inflammatory Cytokines in Lipopolysaccharide (LPS)-Activated Macrophages via NF-κB and Mitogen Activated Protein Kinase (MAPK) Pathways.

BACKGROUND This study aimed to investigate the effects of recombinant human brain natriuretic peptide (rhBNP) on IL-6, TNF-α, and IL-10 secretion in LPS-activated RAW 264.7 cells and human peripheral blood mononuclear cells (PBMCs) in vitro and to explore the related signaling pathways of the regulation mechanisms of BNP in systemic inflammatory response syndrome (SIRS). MATERIAL AND METHODS MTT assay was used to evaluate the effects of rhBNP on cell viabilities. Lipopolysaccharide (LPS) was used to induce inflammation response. The whole study was divided into 8 groups: Control, low, middle, and high concentrations of rhBNP, LPS, LPS with low, middle, and high concentrations of rhBNP. Levels of IL-6, TNF-α, and IL-10 were evaluated using the Cytometric Bead Array Kit and RT-PCR assay. Western blotting was used to test the effects of rhBNP on inflammation-related NF-kB and MAPK pathways. RESULTS Except for the concentrations ≥1.6 ng/mL, all concentrations of rhBNP showed little effect on cell viabilities of RAW264.7 cells and PBMCs after 24 h and 48 h, suggesting a weak cytotoxicity to cells. Expression of IL-6 and TNF-α significantly increased and expression of IL-10 significantly decreased at protein and mRNA levels after LPS treatment, and these effects were strongly inhibited in a dose-dependent manner by pretreatment of rhBNP. Similarly, the LPS-induced increase of NF-kB and MAPK pathway phosphorylation levels were also significantly inhibited by rhBNP. CONCLUSIONS rhBNP can regulate expression of IL-6, TNF-α, and IL-10 in LPS-activated RAW 264.7 cells and PBMCs through inhibiting NF-κB and MAPK pathways. These results may reveal potential causes of the increase of BNP in SIRS and may provide an experimental basis for treatment of SIRS.

The antiepileptic effect of the glycolytic inhibitor 2-deoxy-D-glucose is mediated by upregulation of K(ATP) channel subunits Kir6.1 and Kir6.2.

Metabolic modulation of neuronal excitability is becoming increasingly important as an antiepileptic therapy. It was reported that the glycolytic inhibitor 2-deoxy-D-glucose (2-DG) and the activation of the ATP-sensitive potassium ion channel (K(ATP) channel) had an antiepileptic effect in models of epilepsy. To explore whether 2-DG exerts an antiepileptic effect through upregulation of the K(ATP) channel subunits Kir6.1 and Kir6.2, the expression of these subunits in hippocampus of five groups of mice with pilocarpine-induced status epilepticus (SE) was evaluated. A seizure group with pilocarpine-kindling convulsions (EP) was compared to similar groups treated with high, medium, and low 2-DG concentrations (100-500 mg/kg) and a normal control group (Con). Kir6.1 and Kir6.2 mRNAs and proteins were analyzed at 4 h, 1 days (acute period), 7 days (latent period), 30, and 60 days (chronic period) following SE. In the seizure group (compared to the Con group), hippocampal expression of Kir6.1 and Kir6.2 increased dramatically at 1, 7, and 30 days, and was further increased after treatment with medium and high dose 2-DG (all P < 0.05). Our results suggest that 2-DG may exert an antiepileptic effect through up-regulation of mRNAs and protein levels of Kir6.1 and Kir6.2, which may therefore be used as molecular targets in the treatment of epilepsy with 2-DG.

Glycolysis in energy metabolism during seizures.

Studies have shown that glycolysis increases during seizures, and that the glycolytic metabolite lactic acid can be used as an energy source. However, how lactic acid provides energy for seizures and how it can participate in the termination of seizures remains unclear. We reviewed possible mechanisms of glycolysis involved in seizure onset. Results showed that lactic acid was involved in seizure onset and provided energy at early stages. As seizures progress, lactic acid reduces the pH of tissue and induces metabolic acidosis, which terminates the seizure. The specific mechanism of lactic acid-induced acidosis involves several aspects, which include lactic acid-induced inhibition of the glycolytic enzyme 6-diphosphate kinase-1, inhibition of the N-methyl-D-aspartate receptor, activation of the acid-sensitive 1A ion channel, strengthening of the receptive mechanism of the inhibitory neurotransmitter γ-minobutyric acid, and changes in the intra- and extracellular environment.

The role of local field potential coupling in epileptic synchronization.

THIS REVIEW HOPES TO CLEARLY EXPLAIN THE FOLLOWING VIEWPOINTS: (1) Neuronal synchronization underlies brain functioning, and it seems possible that blocking excessive synchronization in an epileptic neural network could reduce or even control seizures. (2) Local field potential coupling is a very common phenomenon during synchronization in networks. Removal of neurons or neuronal networks that are coupled can significantly alter the extracellular field potential. Interventions of coupling mediated by local field potentials could result in desynchronization of epileptic seizures. (3) The synchronized electrical activity generated by neurons is sensitive to changes in the size of the extracellular space, which affects the efficiency of field potential transmission and the threshold of cell excitability. (4) Manipulations of the field potential fluctuations could help block synchronization at seizure onset.

Expression of connexin 36 in central nervous system and its role in epileptic seizure.

OBJECTIVE: This review discusses the experimental and clinical studies those show the expression of connexin 36 in the central nervous system and the possible role of connexin 36 in epileptic seizure. DATA SOURCES: All articles used in this review were mainly searched from PubMed published in English from 1996 to 2012. STUDY SELECTION: Original articles and reviews were selected if they were related to the expression of connexin 36 in the central nervous system and its role in epilepsy. RESULTS: The distribution of connexin 36 is developmentally regulated, cell-specific and region-specific. Connexin 36 is involved in some neuronal functions and epileptic synchronization. Changes in the connexin 36 gene and protein were accompanied by seizures. Selective gap junction blockers have exerted anticonvulsant actions in a variety of experiments examined in both humans and experimental animals. CONCLUSIONS: Connexin 36 plays an important role in both physiological and pathological conditions in the central nervous system. A better understanding of the role of connexin 36 in seizure activity may contribute to the development of new therapeutic approaches to treating epilepsy.