Sulforaphane enhanced muscle growth by promoting lipid oxidation through modulating key signaling pathways.

Sulforaphane (SFN) has shown diverse effects on human health and diseases. SFN was administered daily to C57BL/6J mice at doses of 1 mg/kg (SFN1) and 3 mg/kg (SFN3) for 8 weeks. Both doses of SFN accelerated body weight increment. The cross-sectional area and diameter of Longissimus dorsi (LD) muscle fibers were enlarged in SFN3 group. Triglyceride (TG) and total cholesterol (TC) levels in LD muscle were decreased in SFN groups. RNA sequencing results revealed that 2455 and 2318 differentially expressed genes (DEGs) were found in SFN1 and SFN3 groups, respectively. Based on GO enrichment analysis, 754 and 911 enriched GO terms in the SFN1 and SFN3 groups, respectively. KEGG enrichment analysis shown that one KEGG pathway was enriched in the SFN1 group, while six KEGG pathways were enriched in the SFN3 group. The expressions of nine selected DEGs validated with qRT-PCR were in line with the RNA sequencing data. Furthermore, SFN treatment influenced lipid and protein metabolism related pathways including AMPK signaling, fatty acid metabolism signaling, cholesterol metabolism signalling, PPAR signaling, peroxisome signaling, TGFß signaling, and mTOR signaling. In summary, SFN elevated muscle fibers size and reduced TG and TC content of in LD muscle by modulating protein and lipid metabolism-related signaling pathways.

A rare case of anti-DPPX encephalitis combined with neuroleptospirosis.

BACKGROUND: Neuroleptospirosis and anti-dipeptidyl-peptidase-like protein 6 (DPPX) encephalitis are both very rare and have only been reported in the form of respective case reports. There are no reports of anti-DPPX encephalitis combined with neuroleptospirosis in the literature. We reported the first case of neuroleptospirosis combined with elevated DPPX antibodies in serum and cerebrospinal fluid (CSF). CASE PRESENTATION: A previously healthy 53-year-old Chinese male farmer with a history of drinking raw stream water and flood sewage exposure was brought to the hospital due to an acute onset of neuropsychiatric symptoms. No fever or meningeal irritation signs were detected on physical examination. Routine laboratory investigations, including infection indicators, leukocyte and protein in CSF, electroencephalogram and gadolinium-enhanced magnetic resonance imaging of the brain, all revealed normal. While metagenomic next-generation sequencing (mNGS) identified the DNA genome of Leptospira interrogans in the CSF. Anti-DPPX antibody was detected both in blood and in CSF. A diagnosis of neuroleptospirosis combined with autoimmune encephalitis associated with DPPX-Ab was eventually made. He resolved completely after adequate amount of penicillin combined with immunotherapy. CONCLUSION: We highlight that in patients with acute or subacute behavioral changes, even in the absence of fever, if the most recent freshwater exposure is clear, physicians should pay attention to leptospirosis. Due to the low sensitivity of routine microscopy, culture, polymerase chain reaction and antibody testing, mNGS may have more advantages in diagnosing neuroleptospirosis. As autoimmune encephalitis can be triggered by various infections, neuroleptospirosis may be one of the causes of autoimmune encephalitis. Since neuronal antibody measurements themselves are not that common in neuroleptospirosis, future studies are needed to determine whether the detection of anti-DPPX antibodies is a rare event in leptospirosis. Early identification of autoimmune encephalitis and timely administration of immunotherapy may lead to a better outcome.

The protective effect of Wnt3a on inflammatory response in oxygen-glucose deprivation/reoxygenation (OGD/R) astrocyte model.

Involving in the immune response after cerebral infarction, astrocytes could secrete large amounts of pro- and anti-inflammatory factors. The aim of this study is to investigate the effect of Wnt3a intervention on the inflammatory response of oxygen-glucose deprivation (OGD) followed by reoxygenation (OGD/R) astrocyte model, and to provide a new target for immunoprotective treatment of cerebral infarction. We constructed the OGD/R rat astrocyte model, the astrocytes were treated by different concentrations of glucose (25, 50, 100 mM) intervened with/without Wnt3a (25 µg/ml). Microscope was used to observe the cell survival in rat astrocytes. The relative expression of inflammatory factors (TNF-a, IL-6, HIF-a) in rat astrocytes was detected by qRT-PCR. The expression of inflammatory factors such as TNF-a, IL-6 and HIF-a in rat astrocytes was increased after OGD/R treatment. The Wnt3a intervention promoted cell survival and decreased the expression of inflammatory factors in rat astrocytes induced by OGD/R. There is a neuroprotective effect that Wnt3a intervention could reduce inflammatory response in the OGD/R rat astrocyte model.

Chinese stroke patients with atrial fibrillation used Robert's age-adjusted warfarin loading protocol obtained good INR results within therapeutic range.

To assess whether Roberts' age-adjusted warfarin loading protocol is effective in Chinese patients and whether the SAMeTT2R2 score can predict international normalized ratio (INR) control. Roberts' protocol for warfarin titration was applied to patients with non-valvular atrial fibrillation (NVAF) complicated with ischemic stroke at the Department of Neurology between 2014 and 2019. Clinical and sociodemographic variables were recorded. A minimum of 1-year follow-up was used to calculate the time in therapeutic range (TTR) of the INR. A total of 94 acute ischemic stroke patients with NVAF were included in the study. Seventy-seven (81.9%) of the patients had attained stable INR (2.0-3.0) at the fifth dose, and 90.0% of the patients had achieved stable INR on the ninth day. Seventeen (18.1%) of the patients had an INR > 4 during dose-adjustment period. Patients with INR > 4 had significantly lower body weight (53.8 vs. 63.1 kg, P = 0.014), lower rate of achievement of stable INR (35.3% vs. 92.2%, P = 0.000), and lower rate of TTR ≥ 65% (23.5% vs. 70.1%, P = 0.001), but with no significant increase in bleeding risk. A total of 89 patients underwent long-term INR follow-up, of which 58 (65.2%) patients achieved TTR ≥ 65%. Patients with poor TTR had significantly lower body weight (56.3 vs. 63.7 kg, P = 0.020) and lower rate of stable INR achievement (64.5% vs. 89.7%, P = 0.002). All 94 patients had SAMeTT2R2 score ≥ 2. There was no linear association between SAMeTT2R2 score and the rate of TTR ≥ 65% (Ptrend = 0.095). Chinese ischemic stroke patients with NVAF on warfarin can safely and quickly achieve therapeutic INR using Roberts' age-adjusted protocol and can obtain a good TTR. Lower body weight may be a predictor of poor TTR and INR > 4. Patients who have not attained stable INR after adjusting the dose five times are at high risk for poor TTR. SAMeTT2R2 score may not predict TTR in Chinese ischemic stroke patients with NVAF.

Synthesis of Single Crystal 2D Cu2FeSnS4 Nanosheets with High-Energy Facets (111) as a Pt-Free Counter Electrode for Dye-Sensitized Solar Cells.

Two-dimensional Cu2FeSnS4 (CFTS) nanosheets with exposed high-energy facets (111) have been synthesized by a facile, scalable, and cost-effective one-pot heating process. The CFTS phase formation is confirmed by both X-ray diffraction and Raman spectroscopy. The formation mechanism of exposed high-energy facet CFTS growth is proposed and its electrochemical and photoelectrochemical properties are investigated in detail to reveal the origin of the anisotropic effect of the high-energy facets. Dye-sensitized solar cells (DSSC) achieve a favorable power conversion efficiency of 5.92% when employing CFTS thin film as a counter electrode, suggesting its potential as a cost-effective substitute for Pt in DSSCs.

Using Sociological Theories and Methods to Analyze the Solutions and Measures of Environmental Pollution Problems.

In order to further improve the effectiveness of environmental pollution control and improve the quality of the atmospheric ecological environment, this article discusses regional environmental pollution control from the perspective of sociological theories and methods. Therefore, the article starts with the characteristics of environmental air pollution, combined with linear regression analysis and PSR model principal component analysis, focuses on the impact factors of environmental pollution, and concludes that the weights of pressure layer, state layer, and response layer for the impact of environmental state are 0.4824, 0.261, and 0.1207, respectively. On this basis, from the perspective of social, collaborative governance, and public management, this article focuses on the political measures of environmental pollution.

Beware of the DeBakey type I aortic dissection hidden by ischemic stroke: Two case reports.

BACKGROUND: DeBakey type I aortic dissection is one of the rare etiologies of ischemic stroke. It is critical to identify arterial dissection before intravenous thrombolysis; otherwise, fatal hemorrhage may occur. CASE SUMMARY: In this report, we described 2 painless DeBakey type I aortic dissection cases with initial symptoms similar to ischemic stroke. Sudden onset of conscious disturbance and limb weakness within minutes occurred in both cases. Hypotension was found in both cases. Thoracoabdominal computed tomography angiography was urgently performed due to unknown reason hypotension, and DeBakey type I aortic dissection was confirmed. Intravenous thrombolysis was avoided because of timely diagnosis; however, they both eventually died of ruptured aortic dissection. CONCLUSION: Aortic dissection should always be excluded in ischemic stroke patients with unexplained hypotension or shock symptoms before intravenous thrombolytic therapy.

Anti-glioblastoma Activity of Kaempferol via Programmed Cell Death Induction: Involvement of Autophagy and Pyroptosis.

Glioblastoma is one of the most common and lethal intracranial malignant, and is still lack of ideal treatments. Kaempferol is a major nutrient found in various edible plants, which has exhibited the potential for the treatment of glioblastoma. However, the specific anti-glioma mechanism of kaempferol is yet to be studied. Herein, we aim to explore the mechanisms underlying the anti-glioma activity of kaempferol. Our results demonstrated that kaempferol suppresses glioma cell proliferation in vitro and inhibits tumor growth in vivo. Moreover, kaempferol raises ROS and decreases mitochondrial membrane potential in glioma cells. The high levels of ROS induce autophagy then ultimately trigger the pyroptosis of glioma cells. Interestingly, when we used 3-MA to inhibit autophagy, we found that the cleaved form of GSDME was also decreased, suggesting that kaempferol induces pyroptosis through regulating autophagy in glioma cells. In conclusion, this study revealed kaempferol possesses good anti-glioma activity by inducing ROS, and subsequently leads to autophagy and pyroptosis, highlighting its clinical potentials as a natural nutrient against glioblastoma.

Tanshinone IIA effects on ovarian cancer cell line.

OBJECTIVES: To explore the potential therapeutic effect of Tanshinone IIA against ovarian cancer in vitro and elucidate the underlying molecular mechanism. METHODS: The cell survival upon Tanshinone IIA treatment was determined by the clonogenic assay. Cell apoptosis was analysed by Annexin V/propidium iodide double staining. The cleaved caspase-3/poly ADP-ribose polymerase and apoptosis-related factors were quantified by Western blotting. The relative expression of microRNAs (miRs) was determined by real-time polymerase chain reaction. KEY FINDINGS: Tanshinone IIA treatment induced significant apoptosis in TOV-21G cells. Tanshinone suppressed survivin expression while not affected Bax, Bcl-2 and Bcl-xL. We further predicted and experimentally confirmed overexpression of miR-205 in TOV-21G, which ectopic significantly inhibited survivin and promoted cell apoptosis. miR-205-specific antagonist completely abrogated the cell suppressive effect of Tanshinone IIA. CONCLUSIONS: Our data suggested that Tanshinone IIA induced cell apoptosis in ovarian carcinoma TOV-21G cells via direct upregulation of miR-205. Our study highlighted the potential therapeutic application of Tanshinone IIA against ovarian malignancy.

Pin1 facilitates isoproterenol­induced cardiac fibrosis and collagen deposition by promoting oxidative stress and activating the MEK1/2­ERK1/2 signal transduction pathway in rats.

Peptidyl­prolyl cis/trans isomerase, NIMA-interacting 1 (Pin1) is a member of a large superfamily of phosphorylation­dependent peptidyl­prolyl cis/trans isomerases, which not only regulates multiple targets at various stages of cellular processes, but is also involved in the pathogenesis of several diseases, including microbial infection, cancer, asthma and Alzheimer's disease. However, the role of Pin1 in cardiac fibrosis remains to be fully elucidated. The present study investigated the potential mechanism of Pin1 in isoprenaline (ISO)­induced myocardial fibrosis in rats. The rats were randomly divided into three groups. Echocardiography was used to evaluate changes in the size, shape and function of the heart, and histological staining was performed to visualize inflammatory cell infiltration and fibrosis. Reverse transcription­quantitative polymerase chain reaction analysis, immunohistochemistry and Picrosirius red staining were used to differentiate collagen subtypes. Additionally, cardiac­specific phosphorylation of mitogen­activated protein kinase kinase 1/2 (MEK1/2) and extracellular­signal regulated protein kinase 1/2 (ERK1/2), and the activities of Pin1 and α­smooth muscle actin (α­SMA) and other oxidative stress parameters were estimated in the heart. The administration of ISO resulted in an increase in cardiac parameters and elevated the heart­to­body weight ratio. Histopathological examination of heart tissues revealed interstitial inflammatory cellular infiltrate and disorganized collagen fiber deposition. In addition, lipid peroxidation products and oxidative stress marker activity in plasma and tissues were significantly increased in the ISO­treated rats. Western blot analysis showed significantly elevated protein levels of phosphorylated Pin1, MEK1/2, ERK1/2 and α­SMA in remodeling hearts. Treatment with juglone following intraperitoneal injection of ISO significantly prevented inflammatory cell infiltration, improved cardiac function, and suppressed oxidative stresses and fibrotic alterations. In conclusion, the results of the present study suggested that the activation of Pin1 promoted cardiac extracellular matrix deposition and oxidative stress damage by regulating the phosphorylation of the MEK1/2­ERK1/2 signaling pathway and the expression of α­SMA. By contrast, the inhibition of Pin1 alleviated cardiac damage and fibrosis in the experimental models, suggesting that Pin1 contributed to the development of cardiac remodeling in ISO­administered rats, and that the inactivation of Pin1 may be a novel therapeutic candidate for the treatment of cardiovascular disease and heart failure.

TRPM7 channels mediate the functional changes in cardiac fibroblasts induced by angiotensin II.

Transient receptor potential melastatin 7 (TRPM7), a bifunctional channel protein owning both cation permeability and kinase activity, plays an important role in the pathophysiological process of many cell types, such as vascular smooth muscle cells, human glioma cells and mouse cortical astrocytes. However, whether TRPM7 channels play a key role in the functional change of cardiac fibroblasts (CFs) induced by angiotensin II (Ang II) remains unknown. Using Cell Counting Kit-8 (CCK-8) assay, immunofluorescence assay, western blot analysis, RT-qPCR, RNA interference (RNAi) and whole-cell patch-clamp techniques, the present study aimed to explore the role of TRPM7 channels in the proliferation, differentiation and collagen synthesis of CFs induced by Ang II. Our data showed that Ang II time-dependently increased TRPM7 expression and TRPM7 currents in the CFs. Downregulation of TRPM7 attenuated the TRPM7 current density, and inhibited the proliferation, differentiation and collagen synthesis of CFs induced by Ang II. Our results identified the TRPM7 channel as a pivotal member associated with the functional change of CFs induced by Ang II, and suggest that the TRPM7 channel may represent a promising therapeutic strategy for the treatment of fibrosis-related cardiac diseases.

Molecular Epidemiological Survey of Glucose-6-Phosphate Dehydrogenase Deficiency and Thalassemia in Uygur and Kazak Ethnic Groups in Xinjiang, Northwest China.

Glucose-6-phosphate dehydrogenase (G6PD) deficiency and thalassemia occur frequently in tropical and subtropical regions, while the prevalence of relationship between the two diseases in Xinjiang has not been reported. We aimed to determine the prevalence of these diseases and clarify the relationship between genotypes and phenotypes of the two diseases in the Uygur and Kazak ethnic groups in Xinjiang. We measured G6PD activity by G6PD:6PGD (glucose acid-6-phosphate dehydrogenase) ratio, identified the gene variants of G6PD and α- and ß-globin genes by polymerase chain reaction (PCR)-DNA sequencing and gap-PCR and compared these variants in different ethnic groups in Xinjiang with those adjacent to it. Of the 149 subjects with molecular analysis of G6PD deficiency conducted, a higher prevalence of the combined mutations c.1311C > T/IVSXI + 93T > C and IVSXI + 93T > C, both with normal enzymatic activities, were observed in the Uygur and Kazak subjects. A case of rare mutation HBB: c.135delC [codon 44 (-C) in the heterozygous state], a heterozygous case of HBB: c.68A > G [Hb G-Taipei or ß22(B4)Glu→Gly] and several common single nucleotide polymorphisms (SNPs) were found on the ß-globin gene. In conclusion, G6PD deficiency with pathogenic mutations and three common α-thalassemia (α-thal) [- -(SEA), -α(3.7) (rightward), -α(4.2) (leftward)] deletions and point mutations of the α-globin gene were not detected in the present study. The average incidence of ß-thalassemia (ß-thal) in Uygurs was 1.45% (2/138) in Xinjiang. The polymorphisms of G6PD and ß-globin genes might be useful genetic markers to trace the origin and migration of the Uygur and Kazak in Xinjiang.

Dual Opposing Roles of Metallothionein Overexpression in C57BL/6J Mouse Pancreatic ß-Cells.

BACKGROUND: Growing evidence indicates that oxidative stress (OS), a persistent state of excess amounts of reactive oxygen species (ROS) along with reactive nitrogen species (RNS), plays an important role in insulin resistance, diabetic complications, and dysfunction of pancreatic ß-cells. Pancreatic ß-cells contain exceptionally low levels of antioxidant enzymes, rendering them susceptible to ROS-induced damage. Induction of antioxidants has been proposed to be a way for protecting ß-cells against oxidative stress. Compared to other antioxidants that act against particular ß-cell damages, metallothionein (MT) is the most effective in protecting ß-cells from several oxidative stressors including nitric oxide, peroxynitrite, hydrogen peroxide, superoxide and streptozotocin (STZ). We hypothesized that MT overexpression in pancreatic ß-cells would preserve ß-cell function in C57BL/6J mice, an animal model susceptible to high fat diet-induced obesity and type 2 diabetes. RESEARCH DESIGN AND METHODS: The pancreatic ß-cell specific MT overexpression was transferred to C57BL/6J background by backcrossing. We studied transgenic MT (MT-tg) mice and wild-type (WT) littermates at 8 weeks and 18 weeks of age. Several tests were performed to evaluate the function of islets, including STZ in vivo treatment, intraperitoneal glucose tolerance tests (IPGTT) and plasma insulin levels during IPGTT, pancreatic and islet insulin content measurement, insulin secretion, and islet morphology assessment. Gene expression in islets was performed by quantitative real-time PCR and PCR array analysis. Protein levels in pancreatic sections were evaluated by using immunohistochemistry. RESULTS: The transgenic MT protein was highly expressed in pancreatic islets. MT-tg overexpression significantly protected mice from acute STZ-induced ROS at 8 weeks of age; unexpectedly, however, MT-tg impaired glucose stimulated insulin secretion (GSIS) and promoted the development of diabetes. Pancreatic ß-cell function was significantly impaired, and islet morphology was also abnormal in MT-tg mice, and more severe damage was detected in males. The unique gene expression pattern and abnormal protein levels were observed in MT-tg islets. CONCLUSIONS: MT overexpression protected ß-cells from acute STZ-induced ROS damages at young age, whereas it impaired GSIS and promoted the development of diabetes in adult C57BL/6J mice, and more severe damage was found in males.

Expression of interleukin-9 and its upstream stimulating factors in rats with ischemic stroke.

To investigate the temporal expressions of IL-9 and its related cytokines after middle cerebral artery occlusion in rats. IL-9 and its related cytokines in ischemia brain and blood were tested after rats were subjected to transient focal ischemia. Comparing with sham-operated group, the levels of IL-4, TGF-ß, PU.1, IRF4, OX40, NIK, RelB-p52 and IL-9 in experimental groups were significantly higher after middle cerebral artery occlusion. The results showed that expressions of IL-9 and its upstream stimulating factors increased in experimental stroke, and whether they play a role or just a secondary change is awaiting further research.

[Analysis of OCRL gene mutation in a male infant with Lowe syndrome].

OBJECTIVE: To identify pathological mutation in a Chinese male infant featuring oculocerebrorenal syndrome (also called Lowe syndrome). METHODS: Clinical data of the patient were collected. DNA was extracted from peripheral blood of the infant and his parents. All of the 24 exons and intron-exon splice sites of OCRL gene were amplified with PCR. Mutations were detected by direct sequencing the PCR products. RESULTS: The infant was found to have carried a c.1499G>A (p.R500Q) mutation in exon 15 of the OCRL gene, which was transmitted from his mother, who was heterozygous for the same mutation. The c.1499G>A mutation, discovered in Chinese population for the first time, has been reported to cause severe Lowe syndrome in other ethnic populations. CONCLUSION: The c.1499G>A mutation of the OCRL gene is probably responsible for the disease in the patient. Further study of this mutation may facilitate delineation of the genotype-phenotype correlation of this disease.

Risk factors and etiological subtype analysis of brainstem infarctions.

OBJECTIVE: To evaluate the features of risk factors and etiological subtypes of brainstem infarctions (BSIs) patients in China. METHODS: One hundred and ninety-nine cerebral infarction patients with brainstem involvement were categorized into five groups according to Trial of Org 10172 in Acute Stroke Treatment classification: large artery disease (LAD), cardioembolism (CE), small vessel disease (SVD), stroke of other determined etiology (SOE) or stroke of undetermined etiology (SUE). The risk factors and percentage of the different etiological subtypes were assessed. RESULT: A total of 199 patients were enrolled in this study. The number and percentage of patients in SVD, LAD, SUE, CE and SOE were 77 (38.7%), 74 (37.2%), 25 (12.6%), 23 (11.6%) and 0, respectively. There were significantly different incidences of hypertension, diabetes and coronary heart disease (CHD) without atrial fibrillation (AF) among different stroke subtypes (P=0.006, P=0.002, P=0.016, respectively). Hypertension was more prevalent in LAD than in SVD and CE (P=0.001 and P=0.039, respectively) while the incidence of diabetes in LAD was higher than those in SVD and CE (P<0.001 and P=0.015, respectively). CHD without AF was more prevalent in CE than in SVD and LAD (P=0.044 and P=0.012, respectively). LAD was significantly associated with hypertension (OR=3.18, P=0.009) and diabetes (OR=2.84, P=0.003) in BSIs. CONCLUSION: The pattern of etiological subtypes of BSIs in China has its own characteristics. It might result from the features of risk factors in Chinese patients.

The Hb H disease genotypes in Southern China.

Abstract We report the genetic data of 435 patients with Hb H (ß4) disease who presented at our center between 2005 and 2012. Our results showed that all patients had the Southeast Asian deletion (- -(SEA)) on one allele. The -α(3.7) (rightward) deletion was the most common on the other allele, followed by the -α(4.2) (leftward) deletion, Hb Constant Spring (Hb CS, α142, Term → Gln; HBA2: c.427T > C) and Hb Quong Sze [Hb QS, α125(H8)Leu → Pro; HBA2: c.377T > C] mutations. Two rare point mutations, α31(B12)Arg → Lys; HBA2: c.95G > A and Hb Zurich Albisrieden [α59(E8)Gly → Arg; HBA1: c.178G > C], were also identified. Four patients had a concomitant ß-thalassemia (ß-thal) heterozygosity. Our results reflect the genetic heterogeneity of Hb H disease and the interaction between Hb H disease and ß-thal trait in Southern China.

Comparison of deep gray matter lesions on magnetic resonance imaging among adults with acute disseminated encephalomyelitis, multiple sclerosis, and neuromyelitis optica.

BACKGROUND: Deep gray matter lesions have been reported in patients with acute disseminated encephalomyelitis (ADEM), multiple sclerosis (MS), and neuromyelitis optica (NMO). OBJECTIVES: The purpose of this study was to compare the features of deep gray matter lesions on magnetic resonance imaging (MRI) among adult patients with ADEM, MS, and NMO. METHODS: Ninety-five adult patients with ADEM (n=12), MS (n=60), and NMO (n=23) who had deep gray matter lesions on MRI were enrolled. Morphological features of deep gray matter lesions among these patients were assessed. RESULTS: Putamen involvement was more common in patients with ADEM than in patients with MS and NMO. Differing from children, thalamus involvement might not be helpful in differentiating ADEM from MS in adults. Hypothalamus involvement was more common in patients with NMO than in patients with ADEM and MS. More importantly, bilateral hypothalamus involvement was more helpful in differentiating NMO from MS. The diameter of the thalamus lesions in patients with ADEM was larger than that in patients with NMO. CONCLUSIONS: Morphological features of deep gray matter lesions vary among adult patients with ADEM, MS, and NMO, and may be helpful in distinguishing these diseases.

Leukoaraiosis and NIHSS score help to differentiate subtypes of intracranial branch atheromatous disease in Southern Han Chinese patients with stroke.

Intracranial branch atheromatous disease (BAD) includes infarcts in the territories of the lenticulostriate arteries (LSA) and paramedian pontine arteries (PPA). The two subtypes of BAD are commonly underused in clinical practice and research. We assessed the clinicoradiologic characteristics of BAD-stroke patients in LSA territories and compared with those of BAD-stroke patients in PPA territories to investigate whether there is a close relationship between leukoaraiosis (LA) and BAD in Southern Han Chinese patients. According to the lesions present in different vascular distributions as shown by diffusion-weighted imaging (DWI), a total of 220 patients diagnosed with BAD, selected from a cohort of 1,458 consecutive patients with acute ischemic stroke, were classified into LSA and PPA groups, comprising 163 and 57 patients, respectively. The characteristics of the patients with BAD were analyzed and differences between the two groups were compared. A high prevalence of concomitant LA (n = 190, 86.36 % of patients with BAD) was observed in the cohort study. Patients in the PPA group had a significantly higher National Institutes of Health Stroke Scale (NIHSS) score on admission than those in the LSA group [6 (4-8) versus 5 (3-7); p = 0.031], and there was a higher prevalence of concomitant LA in the PPA group than the LSA group (96.4 versus 82.8 %; p = 0.010). Conversely, when the number of patients with LA grades ≥ 4 was evaluated, individuals in the LSA group were more frequently affected than those in the PPA group (47.9 versus 31.6 %; p = 0.033). LA showed a high prevalence in Southern Han Chinese patients with BAD. Patients in the LSA group were significantly different from those in the PPA group with respect to NIHSS score, LA and LA grade.

A case of exacerbated multiphasic disseminated encephalomyelitis after interferon ß treatment.

Acute disseminated encephalomyelitis (ADEM) is an inflammatory demyelinating disorder of the central nervous system (CNS), which can be monophasic or with repeated episodes. Relapsing ADEM can be misdiagnosed as multiple sclerosis (MS). We describe here a 16-year-old female patient with multiphasic disseminated encephalomyelitis (MDEM), which was exacerbated after an interferon beta (INF-ß) treatment. The patient presented with polysymptomatic and encephalopathic features at the first attack and was definitively diagnosed with ADEM. During the following 28months, she had two relapses, with the lesions spatially disseminated in time and space, but without encephalopathy. She was diagnosed with MS and started on treatment with IFN-ß injection. A severe relapse occurred 5months after starting IFN-ß treatment, with both the clinical and MRI characteristics worse than during the former 2 relapses, meeting the diagnostic criteria for MDEM. Treatment with IFN-ß was halted, with no new relapses observed over the following 9months. These findings suggest that treating MDEM patients with IFN-ß may exacerbate the disease, similar to that observed during IFN-ß treatment of patients with neuromyelitis optica. Caution should be exercised when treating these patients with IFN-ß.