Prevalence, distribution, accumulation, and risk of environmental corticosteroids and estrogens in biofilms from the Pearl River Delta.

Biofilms play a significant role in the biogeochemical processing of organic matter and the environmental fate of emerging pollutants. In this study, we investigated the occurrence and distribution of 32 endocrine-disrupting chemicals (EDCs), including 24 environmental corticosteroids (ECs) and 8 environmental estrogens (EEs), in natural biofilms from the Pearl River system. Their association between biofilms and water and environmental risk were assessed. The ECs and EEs ubiquitously occurred in the biofilms, ranging from <0.61-6.57 ng/g and <0.8-2535 ng/g, respectively. Temporally, there was no obvious variance in either ECs or EEs in the biofilms during the winter and summer, and their concentrations exhibited a spatial trend of upward to midstream, descending downstream, and then seaward attenuation at the estuary. For ECs and EEs, the similar levels of field-derived bioconcentration factors (BCFs) (logarithm values: 2.42-2.86 and 2.72-2.98, respectively) and biofilm organic carbon-normalized partitioning coefficients (Kboc) (3.39-3.69 and 3.35-3.95) suggest the comparable potential of accumulation and sorption by biofilms between these two classes of EDCs. In addition, higher values of BCF and Kboc for the EEs were found in winter and were correspondingly comparable to their distribution coefficients (Kd) and Koc derived from suspended particles and sediment, revealing that biofilms are a competitive environmental compartment for capturing EDCs, particularly during the mature period. A positive logKboc-logKow relationship suggests hydrophobic partitioning as a primary interaction mechanism between the biofilm and EEs. Moreover, high risks from biofilm-associated ECs and EEs might have posed to the fluvial ecosystem. This study provides original insights into the occurrence, fate, and risk of ECs in natural biofilms for the first time and demonstrates that biofilms may not only serve as reservoirs but also serve as sentinels for fluvial EDC contamination. These results contribute to the further understanding of the behavior and fate of EDCs in aquatic environments.

Effects of the transcription factor Olig1 on the differentiation and remyelination of oligodendrocyte precursor cells after focal cerebral ischemia in rats.

The differentiation and maturation of oligodendrocyte precursor cells (OPCs) is important for remyelination in the central nervous system. Nevertheless, this process is often limited and incomplete in ischemic injury. Oligodendrocyte transcription factor 1 (Olig1) is important for the maturation of OPCs and the repair of demyelinated lesions. However, how Olig1 modulates the development of OPCs or the remyelination associated with ischemic injury remains unclear. The present study aimed to examine alterations in OPCs, and the expression of myelin and Olig1, at different time-points after focal cerebral ischemia using immunohistochemistry and western blot techniques to elucidate the role of Olig1 in the maturation of OPCs and remyelination. The present results showed that the expression of Olig1 significantly decreased at 1 day after middle cerebral artery occlusion (MCAO) and returned to normal levels from day 3 to 28. Additionally, Olig1 was found to translocate into the nucleus following ischemia in the brain. The number of OPCs in the ischemic striatum significantly declined at days 1 and 3 following MCAO, and increased at days 7, 14 and 28 compared with the control. The expression of myelin basic protein, a marker of mature oligodendrocytes and myelin, gradually decreased from day 1 to 7 after ischemia and recovered at day 14 and 28; however, the levels were lower than those in the control group. The present results indicated that the restored normal level of Olig1 following ischemia may play an important role in the maturation of OPCs through its translocation into the nucleus, where it may promote the growth and development of myelin under pathological conditions. However, this endogenous recovery mechanism fails to fully repair the demyelinated lesion. The data of the present study may help clinicians understand the expression pattern of Olig1 and its potential role in endogenous remyelination after ischemia, which may have implications for the treatment of diseases that lead to demyelination.

[Research progress on pathogenesis of temporary osteoporosis in hip].

Transient osteoporosis of the hip(TOH) is classified as a type of bone marrow edema syndrome. TOH is lack of previous study and there is still controversy about his pathogenesis. In recent years, with the development of multi-discipline, such as imaging, pathology, molecular biology, the study has found that the pathological mechanism is complex, while its mechanism is still not clear, which need further research. This paper summarizes the research progress on the pathogenesis of TOH from neurogenic, osteonecrosis, abnormal vascular function, subchondral fracture, heredity and regional acceleration and son on.

[Clinical observation of proximal femoral anti-rotation nail for the treatment of femoral intertrochanteric fracture].

OBJECTIVE: To explore the curative effect and the recessive loss of blooding of PFNA for the treatment of intertrochanteric fractures of femur. METHODS: From January 2012 to January 2015, a total of 49 patients with intertrochanteric fractures of femur were treated with proximal femoral anti-rotation nail including 41 males and 8 females with an average age of 79 years old ranging from 65 to 91 years old. According to the modified Evans type, 1 case was type I, 12 cases were type II, 36 cases were type III. All cases were fresh fractures. Patients had hip pain, movement limited, joint swelling, bruising, extorsion deformity, X-ray and CT examination showed completely fractures. All patients were treated by closed reduction and PFNA internal fixation. Three comminuted fractures using closed reduction were not satisfied, then were treated by limited PFNA fixation after open reduction. RESULTS: The patients' incision got the grade A healing, no complications such as infection and internal fixation failure happened. All patients were followed up from 6 to 36 months (means 22 months). The pain VAS score decreased from preoperative 7.70±1.97 to 1.00±0.26 at 6 months after operation(P<0.01). Harris hip score improved from preoperative 8.70±4.19 to 91.70±5.31 at 6 months after operation(P<0.01). The outcome at 6 months after operation was excellent in 34 cases, good in 7, poor in 1. The fracture healing time was from 8 to 16 weeks with an average of 12 weeks after operation. One patient with osteoporosis, crushing broken, poor compliance, associated with schizophrenia at the same time, appeared with the displacement of the femoral greater trochanter, with conservative treatment for healing. CONCLUSIONS: Intertrochanteric fractures of femur are common in the elderly trauma, in pain relief, recovery of hip function, to provide quality of life for the patients, PFNA achieved satisfactory effect, but its existence is worth to pay close attention to the recessive loss of blood.

Cognitive improvement of mice induced by exercise prior to traumatic brain injury is associated with cytochrome c oxidase.

Though the evidence demonstrated that voluntary exercise programs could be implemented to enhance recovery of cognitive function induced by traumatic brain injury (TBI), the exact mechanisms were still not known. We proposed that the cognitive improvement induced by exercise in TBI mice is associated with cytochrome c oxidase (COX). To demonstrate this hypothesis, adult mice were housed with or without access to a running wheel (RW) for three weeks followed by TBI operation. Acquisition of spatial learning and memory retention was assessed by using the Morris Water Maze (MWM) on days 15 post TBI. The synaptic density was measured by Golji staining. Immunohistochemistry (IHC) for NeuN, GFAP and growth associated protein 43 (GAP43) were also performed. Using Western blot, the expressions of COX I, II, III, BDNF, synapsin I, synaptophysin (SYP) and GAP43 in hippocampus of TBI mice were determinated. Lastly, CcO activity and ATP amount were also detected. Results showed that voluntary exercise prior TBI: (i) counteracted the cognitive deficits and neuron and synaptic density loss associated with the injury; (ii) increased the levels of COX I, II, III, BDNF, synapsin I, SYP and GAP43; (iii) switched the mitochondrial CcO activity and ATP amounts. These studies demonstrated that the COX plays an important role in exercise's cognitive effects in TBI model and also provide evidence that RW training is a promise exercise for traumatically injured mice.

An 85-year-old woman with Miller Fisher syndrome.

Miller Fisher's syndrome (MFS) commonly presents in the fourth and fifth decades and are rare in people over 70 years. An 85-year-old female with no significant medical history presented with upper extremity anesthesia, ptosis, and unsteady gait. The patient had a history of hypertension and diabetes mellitus. Physical examination showed bilateral total external ophthalmoplegia, areflexia, and cerebellar ataxia. Radiological and laboratory studies were unremarkable. Lumbar puncture showed albuminocytological dissociation. The combined history, physical examination, and lumbar puncture results established a presumptive diagnosis of MFS. Intravenous immunoglobulin was given for 5 days. The patient gradually improved 10 days after the onset of symptoms. Ophthalmoplegia had fully recovered after 6 months. To the best of our knowledge, this case represented the oldest patient with MFS.

Enhancing the bioactivity of Poly(lactic-co-glycolic acid) scaffold with a nano-hydroxyapatite coating for the treatment of segmental bone defect in a rabbit model.

PURPOSE: Poly(lactic-co-glycolic acid) (PLGA) is excellent as a scaffolding matrix due to feasibility of processing and tunable biodegradability, yet the virgin scaffolds lack osteoconduction and osteoinduction. In this study, nano-hydroxyapatite (nHA) was coated on the interior surfaces of PLGA scaffolds in order to facilitate in vivo bone defect restoration using biomimetic ceramics while keeping the polyester skeleton of the scaffolds. METHODS: PLGA porous scaffolds were prepared and surface modification was carried out by incubation in modified simulated body fluids. The nHA coated PLGA scaffolds were compared to the virgin PLGA scaffolds both in vitro and in vivo. Viability and proliferation rate of bone marrow stromal cells of rabbits were examined. The constructs of scaffolds and autogenous bone marrow stromal cells were implanted into the segmental bone defect in the rabbit model, and the bone regeneration effects were observed. RESULTS: In contrast to the relative smooth pore surface of the virgin PLGA scaffold, a biomimetic hierarchical nanostructure was found on the surface of the interior pores of the nHA coated PLGA scaffolds by scanning electron microscopy. Both the viability and proliferation rate of the cells seeded in nHA coated PLGA scaffolds were higher than those in PLGA scaffolds. For bone defect repairing, the radius defects had, after 12 weeks implantation of nHA coated PLGA scaffolds, completely recuperated with significantly better bone formation than in the group of virgin PLGA scaffolds, as shown by X-ray, Micro-computerized tomography and histological examinations. CONCLUSION: nHA coating on the interior pore surfaces can significantly improve the bioactivity of PLGA porous scaffolds.

Fermentative hydrogen production from molasses wastewater in a continuous mixed immobilized sludge reactor.

A novel continuous mixed immobilized sludge reactor (CMISR) containing activated carbon as support carrier was used for fermentative hydrogen production from molasses wastewater. When the CMISR system operated at the conditions of influent COD of 2000-6000mg/L, hydraulic retention time (HRT) of 6h and temperature of 35°C, stable ethanol type fermentation was formed after 40days operation. The H(2) content in biogas and chemical oxygen demand (COD) removal were estimated to be 46.6% and 13%, respectively. The effects of organic loading rates (OLRs) on the CMISR hydrogen production system were also investigated. It was found that the maximum hydrogen production rate of 12.51mmol/hL was obtained at OLR of 32kg/m(3)d and the maximum hydrogen yield by substrate consumed of 130.57mmol/mol happened at OLR of 16kg/m(3)d. Therefore, the continuous mixed immobilized sludge reactor (CMISR) could be a promising immobilized system for fermentative hydrogen production.

Anti-N-methyl-D-aspartate receptor encephalitis with serum anti-thyroid antibodies and IgM antibodies against Epstein-Barr virus viral capsid antigen: a case report and one year follow-up.

BACKGROUND: Anti-N-methyl-D-aspartate receptor encephalitis is an increasingly common autoimmune disorder mediated by antibodies to certain subunit of the N-methyl-D-aspartate receptor. Recent literatures have described anti-thyroid and infectious serology in this encephalitis but without follow-up. CASE PRESENTATION: A 17-year-old Chinese female patient presented with psychiatric symptoms, memory deficits, behavioral problems and seizures. She then progressed through unresponsiveness, dyskinesias, autonomic instability and central hypoventilation during treatment. Her conventional blood work on admission showed high titers of IgG antibodies to thyroglobulin, thyroid peroxidase and IgM antibodies to Epstein-Barr virus viral capsid antigen. An immature ovarian teratoma was found and removal of the tumor resulted in a full recovery. The final diagnosis of anti-N-methyl-D-aspartate receptor encephalitis was made by the identification of anti-N-methyl-D-aspartate receptor antibodies in her cerebral spinal fluid. Pathology studies of the teratoma revealed N-methyl-D-aspartate receptor subunit 1 positive ectopic immature nervous tissue and Epstein-Barr virus latent infection. She was discharged with symptoms free, but titers of anti-thyroid peroxidase and anti-thyroglobulin antibodies remained elevated. One year after discharge, her serum remained positive for anti-thyroid peroxidase and anti-N-methyl-D-aspartate receptor antibodies, but negative for anti-thyroglobulin antibodies and IgM against Epstein-Barr virus viral capsid antigen. CONCLUSIONS: Persistent high titers of anti-thyroid peroxidase antibodies from admission to discharge and until one year later in this patient may suggest a propensity to autoimmunity in anti- N-methyl-D-aspartate receptor encephalitis and support the idea that neuronal and thyroid autoimmunities represent a pathogenic spectrum. Enduring anti-N-methyl-D-aspartate receptor antibodies from admission to one year follow-up but seroreversion of Epstein-Barr virus viral capsid antigen IgM may raise the important issue of elucidating the triggers and boosters of anti- N-methyl-D-aspartate receptor encephalitis.

The dose-effect of icariin on the proliferation and osteogenic differentiation of human bone mesenchymal stem cells.

Icariin had been reported as a potential agent for osteogenesis, but the dose-effect relationship needed further research to realize the clinical application of icariin. We isolated and purified human bone mesenchymal stem cells (hBMSCs) and stimulated them with different concentrations of icariin. The cytotoxicity of icariin was evaluated by the methylthiazolytetrazolium (MTT) assay method. The proliferation and osteogenic differentiation of such hBMSCs were investigated for different concentrations of icariin. We found that icariin had a dose-dependent effect on the proliferation and osteogenic differentiation of hBMSCs in a suitable concentration range from 10(-9) M to 10(-6) M, but at concentrations above 10(-5) M, the cytotoxicity limited its use. The extremely low cost of icariin and its high abundance make it appealing for bone regeneration.

Up-regulation of TGF-ß1 mRNA expression in peripheral blood mononuclear cells of patients with chronic fatigue syndrome.

BACKGROUND/PURPOSE: It has been shown that the abnormality in immune cells in chronic fatigue syndrome (CFS) patients is closely associated with the participation of TGF-ß. In order to study the relationship between TGF-ß1 and CFS, we investigated the mRNA levels of TGF-ß1 in peripheral blood mononuclear cells (PBMCs) in patients with CFS. METHODS: Fluorescent quantitative real time reverse-transcription polymerase chain reaction (FQ-RT-PCR) was performed to test TGF-ß1 mRNA expression in PBMCs in 63 cases of CFS, 50 cases of disease controls, and 50 cases of healthy controls. RESULTS: The mean value of TGF-ß1 mRNA expression in CFS patients was ΔΔCt=1.17±0.58, which was significantly higher than the disease controls (ΔΔCt=0.07±1.08, df=111, p < 0.01) and the healthy controls (ΔΔCt=0.00±1.63, df=111, p < 0.01). No significant difference was detected between disease and healthy controls (p > 0.05). CONCLUSION: The expression of TGF-ß1 in PBMCs is significantly elevated in patients with CFS. It might be correlated to the pathogenesis of the disease.

Association between HLA-DRB1 and myasthenia gravis in a northern Han Chinese population.

The cause of myasthenia gravis (MG) is unknown, but it is widely believed to be an autoimmune disease occurring in genetically susceptible individuals. The human leukocyte antigen (HLA) region is considered to be the most important genetic region for MG susceptibility genes. To investigate the association between HLA-DRB1 and myasthenia gravis (MG) in a northern Han Chinese population, a polymerase chain reaction with sequence-specific oligonucleotide probe hybridization method was used to determine the HLA-DRB1 genotypes of 91 patients with MG and 171 healthy individuals. We found that the HLA-DRB1(*)09 allele was significantly more prevalent among patients with MG than among healthy controls, especially those who experienced early onset of the disease (≤40 years), those who were seronegative for acetylcholine receptor antibody, and those with ocular MG. The prevalence of the HLA-DRB1(*)08 allele was significantly lower among patients with MG than among controls. These results indicate that HLA-DRB1(*)09 might be positively associated and DRB1(*)08 negatively associated with MG in the northern Han Chinese population.

Human cytomegalovirus-IgM seropositivity is not associated with atherogenic alterations of lipid profiles and inflammatory status in ischemic stroke patients: a preliminary study.

BACKGROUND: Past exposure to human cytomegalovirus has been suggested to participate in the pathogenetic events associated with atherosclerotic lesion establishment and progression. However, whether ongoing human cytomegalovirus infection is related to plaque instability, and subsequent acute cerebral ischemia, is relatively unknown. The purpose of this study was to evaluate the potential relationships between active human cytomegalovirus infection and ischemic stroke, especially in regard to metabolism and inflammation. METHODS: Ninety-nine acute ischemic stroke patients, associated with large artery atherosclerosis, were divided into two groups based on the presence or absence of human cytomegalovirus immunoglobulin M (IgM) (human cytomegalovirus-IgM-positive/human cytomegalovirus-IgM-negative = 33:66). Baseline clinical characteristics, inflammatory factors, and biochemical assessments were compared in both groups. Then, all patients and human cytomegalovirus-IgM-positive patients were divided into quartiles according to their high-sensitivity C-reactive protein levels, respectively, and risk factors were compared. Finally, correlations between inflammatory factors (high-sensitivity C-reactive protein and white blood cell count) and other atherosclerosis risk factors in both human cytomegalovirus-IgM-positive and -negative subjects were evaluated. RESULTS: An association between human cytomegalovirus-IgM seropositivity and atherogenic modification of metabolism and inflammatory status were not found in this study. Both age and white blood cell count increased across quartiles of high-sensitivity C-reactive protein in all subjects (P = 0.001), while age and low-density lipoprotein cholesterol increased across quartiles of high-sensitivity C-reactive protein in the human cytomegalovirus-IgM-positive group (P = 0.02 and 0.007, respectively). Multivariate linear regression analysis showed that high-sensitivity C-reactive protein was associated with age in human cytomegalovirus-IgM-positive group (P = 0.002), while no other factor was associated with white blood cell count in these subjects. CONCLUSION: Our study provided no evidence for the direct implication of active systemic human cytomegalovirus infection, represented by human cytomegalovirus-IgM positivity, in the pathogenesis of acute ischemic strokes, particularly those involving plaque instability and metabolic disorders.

[Expression of tau-related protein in spinal cord of patients with Alzheimer's disease].

OBJECTIVE: To study the expression of tau-related protein in spinal cord of Chinese patients with Alzheimer's disease. METHODS: Gallays-Braak stain and immunohistochemical study for tau protein (AT8) were carried out in the spinal cord tissue (T2, T8, T10, L2 and S2 segments) of 3 Chinese patients with Alzheimer's disease. Seven age-matched cases without evidence of dementia or neurologic disease were used as controls. RESULTS: Neurofibrillary tangles were identified in the neurons of anterior horn in 2 Alzheimer's disease cases but none was observed in the controls. Tau-positive axons and astroglia were detected in all Alzheimer's disease cases. Tau immunoreactivity in spinal cord of the patients correlated with that in brain tissue. CONCLUSION: The expression of tau-related protein is demonstrated in the spinal cord of Alzheimer's disease patients suggesting that axonal transport defect may play a role in the pathogenesis of Alzheimer's disease.

Clinical, histopathological and genetic studies in a family with fatal familial insomnia.

We compared clinical data from two related Chinese patients with fatal familial insomnia (FFI) and collected information about their pedigree. The clinical features in the two cases were similar and included initial progressive insomnia and sympathetic activation, which persisted throughout the clinical course. A total of 135 members of this family, across seven generations, were retrospectively investigated. Eleven family members, including the two FFI cases, were found to have died with similar neurological problems. Analysis of PRNP in 32 family members revealed eleven carrying the D178N allele, including the two FFI patients. Spongiform degeneration in brains was not found, but gliosis was obvious in the thalamus of the two cases at postmortem. Proteinase K-resistant prion protein (PrP) was not found in proband's brain by immunohistochemistry, but observed in some areas of brain for both cases by PrP-specific Western blot. Investigation of the pedigree has led to the identification of an additional 9 family members who had similar clinical symptoms and 9 currently healthy individuals with the D178N mutation.

[Fluvastatin's effect on atherogenesis in apolipoprotein-E knockout mice infected by cytomegalovirus].

OBJECTIVE: The goal of this study was to investigate whether murine cytomegalovirus (MCMV) is able to exacerbate the atherosclerotic process in apolipoprotein E knockout (apoE -/-) mice, and the effect of fluvastatin on the atherogenesis. METHODS: The apoE-/- mice kept on a west diet were given low dosage of MCMV. At 14,18 and 24 weeks post infection, AS lesion were measured on aorta. The fluvastatin was administered, and AS lesion were measured accordingly above. RESULTS: We observed that in the chronic phase of the infection, AS lesion area was significantly increased. MCMV gB mRNA was not amplified by real-time PCR from the arterial wall. The IgG antibody level of MCMV in blood plasma and the content of virus DNA in salivary gland were not correlated with AS lesions. After the administration of fluvastatin, there was no significant difference of AS lesions between MCMV infected group and mock-infected group. CONCLUSION: MCMV may aggravate the AS lesion in apoE -/- mice in the chronic phase of infection, and promote more severe type of AS lesions. But it might not be the direct effects of mechanism of MCMV on the local lesion of AS. Fluvastatin could meliorate the progression of AS after MCMV infection, but this was not accomplished by decreasing MCMV duplication.

[Studies on heredity rule of the first genealogy regarding fatal familial insomnia in Henan province].

OBJECTIVE: To investigate the epidemiological, genealogic characteristic, familial history of the families with fatal familial insomnia, its clinical and pathological features as well as the heredity rule of related genes. METHODS: 135 familial members of 7 eras were studied. Vein blood samples from patients as well as from some familial members were collected. PRNP gene was studied with PCR, its serial was determined and then authenticated with Nsp I . Brain tissue was obtained for neuropathological test and PrP(Sc) test with Western blot method. RESULTS: Clinical symptoms of the 2 diagnosed cases were typical. 11 familial members died of similar neural disease. 32 samples of their familial members, codon at D178N of PRNP of 11 members was mutated, with mutation rate as 34.38% while D129N showed as methionine. Brain tissue of both probands denaturalized into spongiform and the nerve fiber was absent but PrP(Sc) protein was identified. CONCLUSION: Genealogy was described in the family with fatal familial insomnia since the patients had typical clinical symptoms and pathological characteristics. It seemed necessary to confirm cases of fatal familial insomnia and their genealogy with epidemiological data and to investigate its gene characteristics as well as with neuropathological and Western blot tests.

[Analysis of 62 adult patients with viral meningitis].

OBJECTIVE: To investigate the clinical manifestation, cerebrospinal fluid (CSF) and auxiliary examination findings of adult viral meningitis. METHODS: 62 adult patients with viral meningitis were retrospectively analyzed. RESULTS: Headache occurred in all the 62 (100%) patients, fever occurred in 61 (98%) patients, meningeal irritation sign occurred in 48 (77%) patients. The abduction of left eye was limited in one patient. Seizure occurred in 2 patients. The mean duration time was 17 days, 93% patients less than 30 days. The pressure of CSF increased in 80% patients, leukocyte counts increased in 91% patients, protein level increased in 81% patients, chloride level was normal in 35% patients and slightly lower in 65% patients, glucose level was normal in 94% patients. 7 patients had positive IgM antibody of Coxackievirus B group both in serum and CSF, one patient had positive IgM antibody of EB virus in CSF. Cranial CT scan had no special findings in all patients. 23 patients performed MRI examination, meningeal enhancement occurred in 9 patients. 52% patients had abnormal EEG, mainly increased local or diffuse slow waves. CONCLUSION: Adult viral meningitis was a kind of self-limited disease, chloride level was slightly lower in more than half patients, meningeal enhancement was detected in MRI in part patients.

A patient with Creutzfeldt-Jakob disease with an insertion of 7 octa-repeats in the PRNP gene: molecular characteristics and clinical features.

BACKGROUND: We evaluated the features of neuropathology, abnormal prion protein (PrP) molecules, and clinical data of a Chinese woman diagnosed with familiar Creutzfeldt-Jakob disease (CJD), having 7 octa-repeats inserted with codon 129 methionine homozygote in the PRNP gene. METHODS: Neuropathologic characteristics of the brain were analyzed by hemotoxylin-eosin stain and electronic microscopy. The presence of abnormal PrP in brains was detected by proteinase K and PrP molecules were evaluated by deglycosylation assay. RESULTS: Spongiform degeneration, with diffuse neuronal loss and mild astrocytic gliosis, as well as with profound degeneration of neurons and astrocytes was observed. Proteinase K-resistant PrP was deposited widely in various regions of the brain. Calculation of the glycosylation ratios of proteinase K-resistant PrP molecules identified that the monoglycosyl isomer was predominant. PrP deglycosylation tests allowed for the identification of a predominant 19-kDa PrP signal that represents a partially proteolytic C-terminal segment, a 27-kDa band that represents the full-length wild-type PrP molecule, and a 30-kDa band that probably corresponds to the full-length mutant PrP molecule. CONCLUSION: : Sporadic CJD-like neuropathologic changes and deposits of proteinase K-resistant PrP have been identified in this familiar CJD case with a 168 base pair nucleotide insertion. The clinical features differ from previously reported cases that had 7 octa-repeat insertion, but bear similarities to sporadic CJD.

Detection of human cytomegalovirus in atherosclerotic carotid arteries in humans.

BACKGROUND/PURPOSE: Atherosclerosis plays an important role in stroke. A microbiological infection has been suggested to be involved in the pathogenesis of atherosclerosis, in particular the human cytomegalovirus (HCMV). The objective of this study was to determine the association between HCMV infection and atherosclerosis of the internal carotid arteries in patients of Chinese Han ethnicity with ischemic stroke. METHODS: HCMV DNA and antigen were detected in atherosclerotic internal carotid arteries from 35 patients with ischemic stroke and 20 controls from a Chinese Han ethnic population. Immunohistochemistry, in situ hybridization and polymerase chain reaction were used to detect the HCMV immediate early (IE) and late (L) antigen as well as DNA in the vascular walls. RESULTS: We observed that the proportion of cases that tested positive for HCMV IE but not L antigen and DNA was statistically greater in stroke patients compared with the control population. CONCLUSION: HCMV IE antigen and DNA were associated with the pathological process of atherosclerosis. The vessel wall might be the infection site of the dormant virus.