Hepatitis E virus ORF3 protein hijacking thioredoxin domain-containing protein 5 (TXNDC5) for its stability to promote viral particle release.

Hepatitis E virus (HEV) is the most common cause of acute viral hepatitis worldwide, responsible for approximately 20 million infections annually. Among the three open reading frames (ORFs) of the HEV genome, the ORF3 protein is involved in virus release. However, the host proteins involved in HEV release need to be clarified. In this study, a host protein, thioredoxin domain-containing protein 5 (TXNDC5), interacted with the non-palmitoylated ORF3 protein by co-immunoprecipitation analysis. We determined that the overexpression or knockdown of TXNDC5 positively regulated HEV release from the host cells. The 17FCL19 mutation of the ORF3 protein lost the ability to interact with TXNDC5. The releasing amounts of HEV with the ORF3 mutation (FCL17-19SSP) were decreased compared with wild-type HEV. The overexpression of TXNDC5 can stabilize and increase ORF3 protein amounts, but not the TXNDC5 mutant with amino acids 1-88 deletion. Meanwhile, we determined that the function of TXNDC5 on the stabilization of ORF3 protein is independent of the Trx-like domains. Knockdown of TXNDC5 could lead to the degradation of ORF3 protein by the endoplasmic reticulum (ER)-associated protein degradation-proteasome system. However, the ORF3 protein cannot be degraded in the knockout-TXNDC5 stable cells, suggesting that it may hijack other proteins for its stabilization. Subsequently, we found that the other members of protein disulfide isomerase (PDI), including PDIA1, PDIA3, PDIA4, and PDIA6, can increase ORF3 protein amounts, and PDIA3 and PDIA6 interact with ORF3 protein. Collectively, our study suggested that HEV ORF3 protein can utilize TXNDC5 for its stability in ER to facilitate viral release. IMPORTANCE: Hepatitis E virus (HEV) infection is the leading cause of acute viral hepatitis worldwide. After the synthesis and modification in the cells, the mature ORF3 protein is essential for HEV release. However, the host protein involved in this process has yet to be determined. Here, we reported a novel host protein, thioredoxin domain-containing protein 5 (TXNDC5), as a chaperone, contributing to HEV release by facilitating ORF3 protein stability in the endoplasmic reticulum through interacting with non-palmitoylated ORF3 protein. However, we also found that in the knockout-TXNDC5 stable cell lines, the HEV ORF3 protein may hijack other proteins for its stabilization. For the first time, our study demonstrated the involvement of TXNDC5 in viral particle release. These findings provide some new insights into the process of the HEV life cycle, the interaction between HEV and host factors, and a new direction for antiviral design.

Geographic differences in pharmacotherapy patterns and outcomes of acute ischemic stroke in China.

BACKGROUND: Vast economic and healthcare status discrepancies exist among regions in China, contributing to different treatment patterns. This study was aimed to investigate the current status of pharmacotherapy for acute ischemic stroke (AIS) and outcomes in China and explore the geographic variation in stroke care. METHODS: This study was a multicenter prospective registry study, which collected the data of patients with AIS from 80 hospitals in 46 cities in 2015-2017 across China. Poor functional outcome defined as a modified Rankin Scale score of 3-6 was assessed at 3 and 12 months. Multivariate logistic regression was used. RESULTS: Among 9973 eligible patients, the number of receiving intravenous thrombolysis (IVT), antiplatelet agents, anticoagulants, statin and human urinary kallidinogenase was 429 (4.3%), 9363 (93.9%), 1063 (10.7%), 6828 (74.7%) and 5112 (51.2%), respectively. Multivariable analysis showed IVT use in northeastern was significantly more frequent than in eastern region (OR = 3.17, 95% CI, 2.53-3.99), while the antiplatelets agents use were less frequent (OR = 0.46, 95%CI: 0.38-0.57). The proportions of poor outcomes at 3 and 12 months were 20.7% and 15.8%, respectively. Multivariate analysis showed AIS patients from northeastern and central region had significantly lower risk of poor outcome at month 3 and 12 than those from eastern region (all P < 0.05). CONCLUSIONS: There was a low IVT use and a high antiplatelet agent and statin use for AIS in China. The pharmacotherapy and prognosis of AIS had variation by geographic region. TRIAL REGISTRATION: This study was registered with ClinicalTrials.gov (NCT02470624).

Effect of weekend versus weekday admission on the mortality of acute ischemic stroke patients in China: an analysis of data from the Chinese acute ischemic stroke treatment outcome registry.

Background: Due to disparities in medical resources in rural and urban areas as well as in different geographic regions in China, the effect of weekend versus weekday admission on the outcomes of acute ischemic stroke (AIS) patients is unknown. Our aim was to investigate whether the outcomes of AIS patients differ according to the day of admission in China. Methods: The data were extracted from the Chinese Acute Ischemic Stroke Treatment Outcome Registry (CASTOR), a multicenter prospective study database of patients diagnosed with AIS. The chi-square test (χ2) and logistic regression were used to assess mortality for weekday and weekend admissions among AIS patients stratified by rural or urban status and geographic region (including the eastern, northeastern, central, and western regions). Results: In total, 9,256 patients were included in this study. Of these patients, 57.2% were classified as urban, and 42.8% were classified as rural. A total of 6,760 (73%) patients were admitted on weekdays, and 2,496 (27%) were admitted on weekends. There was no significant difference in the mortality rate among patients admitted on weekends compared with those admitted on weekdays in urban (7.5% versus 7.4%) or rural areas (8.8% versus 8.1%; p > 0.05). The mortality rate was the highest among patients admitted on weekends and weekdays (11.6% versus 10.3%) in the northeastern area, without statistical significance before and after adjusting for the patients' background characteristics (p > 0.05). In addition, regression analysis revealed that the mortality of patients admitted on weekdays was more likely to be influenced by regional subgroup, hospital level and intravenous thrombolysis than that of patients admitted on weekends. Conclusion: The weekend effect was not observed in the mortality of patients with AIS regardless of rural-urban status or geographic region in China.

A new nanobody-enzyme fusion protein-linked immunoassay for detecting antibodies against influenza A virus in different species.

Circulation of influenza A virus (IAV), especially within poultry and pigs, continues to threaten public health. A simple and universal detecting method is important for monitoring IAV infection in different species. Recently, nanobodies, which show advantages of easy gene editing and low cost of production, are a promising novel diagnostic tool for the monitoring and control of global IAVs. In the present study, five nanobodies against the nucleoprotein of H9N2 IAV were screened from the immunized Bactrian camel by phage display and modified with horseradish peroxidase (HRP) tags. Out of which, we determined that H9N2-NP-Nb5-HRP can crossreact with different subtypes of IAVs, and this reaction is also blocked by positive sera for antibodies against different IAV subtypes. Epitope mapping showed that the nanobody-HRP fusion recognized a conserved conformational epitope in all subtypes of IAVs. Subsequently, we developed a nanobody-based competitive ELISA (cELISA) for detecting anti-IAV antibodies in different species. The optimized amount of coating antigen and dilutions of the fusion and testing sera were 100 ng/well, 1:4000, and 1:10, respectively. The time for operating the cELISA was approximately 35 min. The cELISA showed high sensitivity, specificity, reproducibility, and stability. In addition, we found that the cELISA and hemagglutination inhibition test showed a consistency of 100% and 87.91% for clinical and challenged chicken sera, respectively. Furthermore, the agreement rates were 90.4% and 85.7% between the cELISA and commercial IEDXX ELISA kit. Collectively, our developed nanobody-HRP fusion-based cELISA is an ideal method for monitoring IAV infection in different species.

Corrigendum: Screening and identification of nucleocapsid protein-nanobodies that inhibited Newcastle disease virus replication in DF-1 cells.

[This corrects the article DOI: 10.3389/fmicb.2022.956561.].

Screening and identification of nucleocapsid protein-nanobodies that inhibited Newcastle disease virus replication in DF-1 cells.

Newcastle disease (ND) is an acute and highly contagious infectious disease found in poultry. Although commercial ND virus (NDV) vaccines are universally used, some case reports persistently documented vaccination failure. Therefore, novel strategies are still required to control the occurrence of the disease in chickens. Recently, nanobodies (Nbs), which have the advantages of small molecular weight and low production costs, have been shown to be promising therapeutics against viral infection. In the present study, a total of 16 Nbs against NDV nucleocapsid protein (NP) were screened from two libraries against NDV using phage display technology. Of the 16 screened Nbs, eight were prevented from binding to NDV NP protein through administering positive chicken sera for anti-NDV antibodies, indicating that the epitopes recognized by these eight Nbs were able to induce the immune response after the chickens were infected with NDV stock. Subsequently, transfection assay, construction of recombinant DF-1 cells capable of expressing different nanobodies and viral inhibition assay were used to screen the nanobodies inhibiting NDV replication. The results demonstrated that Nb18, Nb30, and Nb88 significantly inhibited the replication of Class I and different genotypes of Class II NDV strains in DF-1 cells when they were expressed in the cytoplasm. Collectively, these nanobodies provided new tools for researching the functions of NDV NP protein and may be used as a novel strategy for designing drugs against NDV infection in chickens.

Regional Differences in Hospital Costs of Acute Ischemic Stroke in China: Analysis of Data From the Chinese Acute Ischemic Stroke Treatment Outcome Registry.

Background and Purpose: Studies on the regional differences in hospital costs of acute ischemic stroke (AIS) are scarce in China. We aimed to explore the regional differences in hospital costs and identify the determinants of hospital costs in each region. Methods: Data were collected from the Chinese Acute Ischemic Stroke Treatment Outcome Registry (CASTOR), a multicenter prospective study on patients diagnosed with AIS and hospitalized from 2015 to 2017. Univariate and multivariate analyses were undertaken to identify the determinants of hospital costs of AIS. Results: A total of 8,547 patients were included in the study, of whom 3,700 were from the eastern area, 2,534 were from the northeastern area, 1,819 were from the central area, and 494 were from the western area. The median hospital costs presented a significant difference among each region, which were 2175.9, 2175.1, 2477.7, and 2282.4 dollars in each area, respectively. Each region showed a similar hospital cost proportion size order of cost components, which was Western medicine costs, other costs, diagnostic costs, and traditional medicine costs, in descending order. Male sex, diabetes mellitus, severe stroke symptoms, longer length of stay, admission to the intensive care unit, in-hospital complications of hemorrhage, and thrombectomy were independently associated with hospital costs in most regions. Conclusion: Hospital costs in different regions showed a similar proportion size order of components in China. Each region had different determinants of hospital costs, which reflected its current medical conditions and provided potential determinants for increasing medical efficiency according to each region's situation.

Predictors and Prognosis of Symptomatic Intracranial Hemorrhage in Acute Ischemic Stroke Patients Without Thrombolysis: Analysis of Data From the Chinese Acute Ischemic Stroke Treatment Outcome Registry.

Background and Purpose: There is limited information on symptomatic intracranial hemorrhage (sICH) in stroke patients without thrombolysis. This study aimed to evaluate the risk factors of sICH and the association between sICH and the prognosis at 3 and 12 months in acute ischemic stroke patients without thrombolysis. Methods: Data originated from the Chinese Acute Ischemic Stroke Treatment Outcome Registry. Univariate analysis and multivariate logistic regression were used to screen the risk factors of sICH. Multivariable logistic regression models were used to assess the association of sICH with poor outcome and all-cause mortality. Results: Totally, 9,484 patients were included, of which 69 (0.73%) had sICH. Atrial fibrillation (odds ratio [OR], 3.682; 95% confidence interval [CI], 1.945-6.971; p < 0.001), history of tumors (OR, 2.956; 95% CI, 1.115-7.593; p = 0.024), and the National Institutes of Health Stroke Scale (NIHSS) score on admission ([6-15: OR, 2.344; 95% CI, 1.365-4.024; p = 0.002] [>15: OR, 4.731; 95% CI, 1.648-13.583; p = 0.004]) were independently associated with sICH. After adjustment of the confounders, patients with sICH had a higher risk of poor outcome (OR, 1.983; 95% CI, 1.117-3.521; p = 0.018) at 3 months and that of all-cause mortality at 3 (OR, 6.135; 95% CI, 2.328-16.169; p < 0.001) and 12 months (OR, 3.720; 95% CI, 1.513-9.148; p = 0.004). Conclusion: sICH occurred in 0.73% of acute ischemic stroke patients without thrombolysis and was associated with a worse prognosis at 3 and 12 months. Atrial fibrillation, history of tumors, and NIHSS score at admission were independent risk factors of sICH.

Ginkgo biloba extract improves cognitive function and increases neurogenesis by reducing Aß pathology in 5×FAD mice.

Previous studies have indicated that the generation of newborn hippocampal neurons is impaired in the early phase of Alzheimer's disease (AD). A potential therapeutic strategy being pursued for the treatment of AD is increasing the number of newborn neurons in the adult hippocampus. Recent studies have demonstrated that ginkgo biloba extract (EGb 761) plays a neuroprotective role by preventing memory loss in many neurodegenerative diseases. However, the extent of EGb 761's protective role in the AD process is unclear. In this study, different doses of EGb 761 (0, 10, 20, and 30 mg/kg; intraperitoneal injections once every day for four months) were tested on 5×FAD mice. After consecutive 4-month injections, mice were tested in learning memory tasks, Aß, and neurogenesis in the dentate gyrus (DG) of hippocampus and morphological characteristics of neurons in DG of hippocampus. Results indicated that EGb 761 (20 and 30 mg/kg) ameliorated memory deficits. Further analysis indicated that EGb 761 can reduce the number of Aß positive signals in 5×FAD mice, increase the number of newborn neurons, and increase dendritic branching and density of dendritic spines in 5×FAD mice compared to nontreated 5×FAD mice. It was concluded that EGb 761 plays a protective role in the memory deficit of 5×FAD mice.

Severe Japanese encephalitis with multiple intracranial hemorrhages: A case report.

RATIONALE: Intracranial hemorrhage occurs infrequently in Japanese encephalitis (JE), and even less frequently with hemorrhage occurring twice. In this report, we describe the clinical features and outcomes of a patient with confirmed JE combined with hemorrhage twice. PATIENT CONCERNS: The patient, a 71-year-old Asian woman, was admitted to the hospital with symptoms of hemiplegia following fever and diarrhea. Soon her condition worsened and a decreased level of consciousness, respiratory failure, and paralysis of extremities occurred.The brain diffusion-weighted imaging sequence showed suspicious abnormal signals in bilateral thalami. Japanese encephalitis virus immunoglobulin M antibody was detected in her serum and cerebrospinal fluid samples, so the patient was diagnosed with JE. During treatment, her condition became aggravated and the brain computed tomography (CT) scan showed multiple lobar hemorrhages. One month later, the multiple lobar hemorrhages occurred again, as observed by a brain CT scan. DIAGNOSIS: JE with multiple intracranial hemorrhages. INTERVENTIONS: The patient was treated comprehensively, including surgery, lowering her intracranial pressure and ventilator-assisted breathing. OUTCOMES: One month later, the patient underwent another surgical procedure for intracranial hemorrhage and suffered a serious neurological disorder. LESSONS: Severe intracranial hemorrhage may occur in elderly patients with JE, especially in those with poor vascular condition. Therefore, when treating such patients, great caution, as well as early detection and prevention, should be taken in case of the occurrence of severe intracranial hemorrhage.

Tangier disease may cause early onset of atherosclerotic cerebral infarction: A case report.

RATIONALE: The present study explored the relationship between the adenosine triphosphate (ATP)-binding cassette A1 (ABCA1) gene, atherosclerosis, and cerebral infarction. The diagnosis and treatment ideas of stroke caused by Tangier disease via the summary of the diagnosis and treatment process of one case with juvenile stroke were explored. The relevant literature on the clinical manifestations, laboratory examinations, and treatment of Tangier disease was reviewed. PATIENT CONCERNS: The brain magnetic resonance imaging (MRI) of a juvenile man with acute onset of sudden right limb weakness and speechlessness revealed infarct lesions. The laboratory tests found low serum high-density lipoprotein (HDL), while further genetic testing identified ABCD1 gene mutation. The mother also carried the mutant gene. DIAGNOSES: Tangier disease was diagnosed. INTERVENTIONS: Statin treatment was administered for platelet aggregation. OUTCOMES: After 3 years of follow-up, the patient was declared to be in a stable condition. LESSONS: ABCA1 gene mutation caused early onset of atherosclerosis, leading to the occurrence of cerebral infarction. The cerebral infarction associated with reduced high-density lipoprotein (HDL), was under intensive focus with respect to ABCA1 gene. Child and Juvenile stroke patients with low HDL should not be excluded from the possibility of Tangier disease.

Headache Secondary to Isolated Sphenoid Sinus Fungus Ball: Retrospective Analysis of 6 Cases First Diagnosed in the Neurology Department.

Fungal sphenoid sinusitis is easily misdiagnosed in clinic, particularly for patients with normal immunological status. Due to the anatomic characteristics of sphenoid sinus, patients presented with various nonspecific symptoms and complications. Headache is the most common presentation, but location of headache is not fixed. We intended to analyze 6 cases of headache secondary to the isolated sphenoid sinus fungus ball (SSFB) which were first diagnosed in the Neurology Department. There was significant female predominance with mean ages of 55 years. They had repeatedly headache history from months to years. The headache was unilateral and usually on the side of lesions. Medication of pain relievers worked well in the beginning of SSFB, but not in the late stage of disease. Notably, all patients did not present positive nervous systemic signs. A preoperative computed tomography (CT) scan or magnetic resonance imaging (MRI) demonstrated the inflammation in sphenoid sinus. Some cases showed calcification in soft tissue or bone lesions of sinus wall. All of 6 patients undertook transnasal endoscopic sphenoidotomy without antifungal therapy after operation. Characteristic fungus ball (FB) was detected after histopathological examination. No headache recurrence was found after average 15.5 months follow-up. Our results suggested that transnasal endoscopic sphenoidotomy is the treatment of choice to remove the FB in sphenoid sinus with a low rate of morbidity and recurrence.

The Effect of Fucoidan on Cellular Oxidative Stress and the CatD-Bax Signaling Axis in MN9D Cells Damaged by 1-Methyl-4-Phenypyridinium.

Background: The purpose of this study was to investigate the impact of fucoidan (FUC) on the oxidative stress response and lysosomal apoptotic pathways in the Parkinson disease (PD) cell model. Methods: The Dopaminergic nerve precursor cell line(MN9D) cells that served as a PD model in this study underwent damage induced by 100 µM 1-methyl-4-phenyl pyridine (MPP+). Cell viability was assessed after FUC treatment and intracellular SOD GSH was measured via immunofluorescence assay. Cellular changes in cathepsin D, Autophagy marker Light Chain 3-II (LC3-II), and apoptotic protein Bax were assessed by Western blot. The expression of Cat D, LC3-II, and B cell lymphoma-2-associated x protein (Bax) was also measured after addition of the cathepsin inhibitor, pepstatin A. Results: The results indicated that MN9D cell viability decreased by 50% within 24 h after 100 µM MPP+ induced toxicity. Pretreatment with 100 µM Fucoidan reduced cellular expression of LC3-II and CatD in 3 h and suppressed the induction of Bax protein. After pepstatin A treatment, Bax expression was significantly downregulated.FUC reversed the reduction of superoxide dismutase (SOD) L-Glutathione(GSH), decreased cell viability, and apoptosis induced by MPP+ in 6 h, suggesting that Fucoidan can attenuate damage to MN9D cells induced by MPP+. Conclusions: Fucoidan protected lysosomes, reduced the expression of LC3-II, inhibited the expression of CatD-Bax and the oxidative stress response, suppressed apoptosis, and thus conferred protective effects for dopaminergic neural cells. FUC may have neuroprotective effects on PD and further research is needed.

Teratoma-associated anti-NMDAR encephalitis: Two cases report and literature review.

OBJECTIVE: This study aimed to discuss the pathogenesis, clinical manifestation, diagnosis, and treatment of anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis. CASE REPORT: The diagnosis and treatment of 2 cases with teratoma-associated anti-NMDAR encephalitis were summarized and the clinical data of patients reported by domestic and international studies were reviewed in this study. The 2 cases were both adolescent females who showed mental abnormalities as their main clinical manifestation. The patients were positive for anti-NMDAR antibody in their serum and cerebrospinal fluid, and gynecologic ultrasound detected ovarian teratoma. After diagnosis, the patients underwent teratoma resection, followed by pulse therapy of hormones and gamma globulin. Chemotherapy was performed to prevent tumor recurrence, and patients were in a stable condition. CONCLUSIONS: Teratoma-associated anti-NMDAR encephalitis is commonly seen in young women. The clinical manifestation of this disease is nonspecific, and the patients mainly have fever, psychosis, and seizure. Tumor resection and immune therapy are effective treatment strategies, and standardized chemotherapy should also be performed to prevent recurrence.

Repetitive transcranial magnetic stimulation for treatment of lactacystin-induced Parkinsonian rat model.

The dysfunction of ubiquitin-proteasome system is an important pathogenesis in the neurodegenerative process of Parkinson's disease. Repetitive transcranial magnetic stimulation (rTMS) is a noninvasive and potential method in treating Parkinson's disease. To investigate whether rTMS has neuroprotective effects in parkinsonian rat model induced by ubiquitin-proteasome system impairment, we gave rTMS daily for 4 weeks to proteasome inhibitor, lactacystin-induced parkinsonian rat model. Rotational behavior test demonstrated that rTMS obviously reduced apomorphine-induced turning number in parkinsonian rats. rTMS could significantly alleviate the loss of tyrosine hydroxylase-positive dopaminergic neurons in lactacystin-lesioned substantia nigra and prevent the loss of striatal dopamine levels. Furthermore, rTMS also reduced the levels of apoptotic protein (cleaved caspase-3) and inflammatory factors (cyclooxygenase-2 and tumor necrosis factor alpha) in lesioned substantia nigra. These results suggest that rTMS can protect nigral dopaminergic neurons against the ubiquitin-proteasome system impairment-induced degeneration by anti-apoptotic and anti-inflammatory molecular mechanism.

Hippocampal infusion of lipopolysaccharide induces immune responses and results in seizures in rats.

Recent studies suggest that epileptic seizures might be facilitated by immune reactions in the brain. However, it remains unclear whether inflammatory reactions could result in acute and chronic epileptic seizures in vivo. In the present study, we investigated whether a hippocampal infusion of lipopolysaccharide (LPS) can induce epileptic seizures in rats. We also aimed to elucidate the molecular mechanisms that underpin this phenomenon. Male Wistar rats received a 1.5 µl infusion of either LPS (5 µg/µl), normal saline, or kainate (KA) (0.4 µg/µl) into the right dorsal hippocampus. No seizures were observed in the normal saline group and associated electroencephalograms showed basic rhythms. Various grades of seizures were observed in rats from the LPS and KA groups, and electroencephalograms were characterized by seizure activities (sharp waves or spikes). In the chronic phase (8 weeks after injection), astrocytes proliferated and the number of neurons decreased in the hippocampus of the rats in the LPS and KA groups. When assessed at the acute phase (within 6 h after injection), the expression of interleukin 1ß, tumor necrosis factor α, and neuronal nitric oxide synthase was significantly increased in the hippocampus of the LPS groups. The results of the present study indicate that hippocampal infusion of LPS can activate innate immune responses of glial cells, thereby inducing epileptic seizures and hippocampal sclerosis in rats.

Alien hand syndrome following corpus callosum infarction: A case report and review of the literature.

Alien hand syndrome (AHS) is characterized by involuntary and autonomous activity of the affected limbs, and consists of the frontal, callosal and posterior AHS variants. The callosal subtype, resulting from damage to the corpus callosum, frequently features intermanual conflict. However, infarction of the corpus callosum is rare due to abundant blood supply. The present study reported a case of AHS (callosal subtype, in the right hand) caused by callosal infarction. Infarction of the left corpus callosum was confirmed with magnetic resonance imaging. In addition, magnetic resonance angiography and digital subtraction angiography examinations revealed multiple lesions in the feeding arteries. Subsequent to antiplatelet therapy for 2 weeks following admission, the patient gradually recovered. Furthermore, the current study reviewed 31 previously reported cases of AHS following callosal infarction in the literature.

Misdiagnosis of a Patient with Internal Carotid Artery Fenestration: A Case Report and Literature Review.

BACKGROUND: Internal carotid artery fenestration is a rare congenital cerebrovascular condition and can be misdiagnosed as carotid artery dissection. CASE REPORT: A patient was initially misdiagnosed with carotid artery dissection. This initial diagnosis was made using a carotid vascular computed angiography and magnetic resonance angiography. A digital subtraction angiography examination revealed a fenestration in the terminal C1 segment of the right internal carotid artery. Previous literature related to carotid artery fenestration was reviewed and analyzed. CONCLUSIONS: Fenestration of the carotid artery combined with aneurysm at the external segment of the internal carotid artery or from the starting position of the carotid artery remains rare in elderly patients, can be misdiagnosed as artery dissection.

Viral encephalitis complicated by acute retinal necrosis syndrome: A case report.

Acute retinal necrosis syndrome (ARN) is a viral infection characterized by focal retinal necrosis. Viral meningitis complicated by ARN is relatively rare. In the present case study, a 44-year-old male presented with fever, headache and mental disorder. After four days, the patient developed blurred vision. The patient was diagnosed with viral encephalitis complicated by bilateral ARN, based on the examination results. After treatment with antivirals and systemic glucocorticoids, the symptoms of the patient improved. Viral encephalitis may be an important risk factor for ARN. For a patient with viral encephalitis who experiences decreased visual acuity or vitreous opacification, the possibility of ARN should be considered.

Significance of Mycobacterium tuberculosis antigen expression in cerebrospinal fluid monocytes in diagnosing tuberculous meningitis.

BACKGROUND: The aim of this study was to investigate the significance of positive expression of Mycobacterium tuberculosis, (MTB) antigen in the cerebrospinal fluid (CSF) monocytes in diagnosing tuberculous meningitis (TBM). MATERIALS AND METHODS: A total of 50 inpatients of TBM, 30 viral meningitis and 20 healthy controls were studied at the 1 st , 2 nd , and 4 th week during their treatment course. Immunohistochemical assay were used to detect early secreted antigenic target 6 (ESAT-6) positive cells, and positive cases were also observed. RESULTS: The percentage of positive cases and positive cells of ESAT-6 in CSF monocytes were all higher in the 1 st and 2 nd week than in the 4 th week in TBM patients (P < 0.01); and percentage of positive cases and positive cells of MTB antigen in CSF monocytes were higher in TBM patients than in viral meningitis and health control in the 1 st and 2 nd week (P < 0.01). The sensitivity was 90% and the specificity was 92% in the early stage (within 2 weeks) of TBM. CONCLUSION: The positive expression of ESAT-6 in CSF monocytes is helpful for the early diagnosis of TBM.