Microglial AIM2 alleviates antiviral-related neuro-inflammation in mouse models of Parkinson's disease.

Inflammasome involvement in Parkinson's disease (PD) has been intensively investigated. Absent in melanoma 2 (AIM2) is an essential inflammasome protein known to contribute to the development of several neurological diseases. However, a specific role for AIM2 in PD has not been reported. In this study, we investigated the effect of AIM2 in the N-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP)-induced PD model by use of various knockout and bone marrow chimeric mice. The mechanism of action for AIM2 in PD was assessed by RNA-sequencing and in vitro primary microglial transfection. Results were validated in the A30P transgenic mouse model of PD. In the MPTP mouse model, AIM2 activation was found to negatively regulate neuro-inflammation independent of the inflammasome. Microglial AIM2 deficiency exacerbated behavioral and pathological features of both MPTP-induced and transgenic PD mouse models. Mechanistically, AIM2 reduced cyclic GMP-AMP synthase (cGAS)-mediated antiviral-related inflammation by inhibition of AKT-interferon regulatory factor 3 (IRF3) phosphorylation. These results demonstrate microglial AIM2 to inhibit the antiviral-related neuro-inflammation associated with PD and provide for a foundation upon which to identify new therapeutic targets for treatment of the disease.

Neuroimaging alterations in dementia with Lewy bodies and neuroimaging differences between dementia with Lewy bodies and Alzheimer's disease: An activation likelihood estimation meta-analysis.

AIMS: The aim of this study was to identify brain regions with local, structural, and functional abnormalities in dementia with Lewy bodies (DLB) and uncover the differences between DLB and Alzheimer's disease (AD). The neural networks involved in the identified abnormal brain regions were further described. METHODS: PubMed, Web of Science, OVID, Science Direct, and Cochrane Library databases were used to identify neuroimaging studies that included DLB versus healthy controls (HCs) or DLB versus AD. The coordinate-based meta-analysis and functional meta-analytic connectivity modeling were performed using the activation likelihood estimation algorithm. RESULTS: Eleven structural studies and fourteen functional studies were included in this quantitative meta-analysis. DLB patients showed a dysfunction in the bilateral inferior parietal lobule and right lingual gyrus compared with HC patients. DLB patients showed a relative preservation of the medial temporal lobe and a tendency of lower metabolism in the right lingual gyrus compared with AD. The frontal-parietal, salience, and visual networks were all abnormally co-activated in DLB, but the default mode network remained normally co-activated compared with AD. CONCLUSIONS: The convergence of local brain regions and co-activation neural networks might be potential specific imaging markers in the diagnosis of DLB. This might provide a pathway for the neural regulation in DLB patients, and it might contribute to the development of specific interventions for DLB and AD.

Reorganization of rich clubs in functional brain networks of dementia with Lewy bodies and Alzheimer's disease.

The purpose of this study was to reveal the patterns of reorganization of rich club organization in brain functional networks in dementia with Lewy bodies (DLB) and Alzheimer's disease (AD). The study found that the rich club node shifts from sensory/somatomotor network to fronto-parietal network in DLB. For AD, the rich club nodes switch between the temporal lobe with obvious structural atrophy and the frontal lobe, parietal lobe and cerebellum with relatively preserved structure and function. In addition, compared with healthy controls, rich club connectivity was enhanced in the DLB and AD groups. The connection strength of DLB patients was related to cognitive assessment. In conclusion, we revealed the different functional reorganization patterns of DLB and AD. The conversion and redistribution of rich club members may play a causal role in disease-specific outcomes. It may be used as a potential biomarker to provide more accurate prevention and treatment strategies.

Predictors and prognoses of epilepsy after anti-neuronal antibody-positive autoimmune encephalitis.

PURPOSE: This study aimed to investigate the incidence and predictors of epilepsy after anti-neuronal antibody-positive autoimmune encephalitis (AIE). The clinical outcomes of patients with epilepsy after AIE were also explored. METHODS: A total of 111 AIE patients were retrospectively evaluated. Post-AIE epilepsy (PAEE) was defined as at least one unprovoked seizure occurring six or more months after discharge from hospital. RESULTS: The incidence of acute symptomatic seizures was 80.2% (89/111) in our AIE patients. Furthermore, of the 89 AIE patients with seizures, 29 (32.6%) presented with seizures as the initial symptom. Overall, 44 out of 111 AIE patients (39.6%) had unprovoked seizures after six months, meeting our definition of PAEE. The independent risk factors for PAEE incidence included an initial presentation with new-onset refractory status epilepticus (NORSE), delayed immunotherapy treatment, the complication of a lung infection during admission, the requirement for mechanical ventilation during hospitalization, parietal lesions observed in magnetic resonance imaging (MRI), and focal slow waves on electroencephalographic (EEG) monitoring. CONCLUSIONS: Early initiation of immunotherapy and lung infection treatment may reduce the risk of conversion of symptomatic seizures to chronic epilepsy in the acute phase of AIE. In general, PAEE patients could have a good prognosis if treated properly and in a timely fashion.

Clinical Characteristics of Cognitive Impairment and 1-Year Outcome in Patients With Anti-LGI1 Antibody Encephalitis.

Introduction: Anti-leucine-rich glioma-inactivated 1 antibody (anti-LGI1) encephalitis is one of the most common autoimmune encephalitis. Anti-LGI1 encephalitis presented with subacute or acute onset of cognitive impairment, psychiatric disturbances, faciobrachial dystonic seizures (FBDSs), convulsions, and hyponatremia. The common sequela of anti-LGI1 encephalitis is cognitive disorder, but there are few studies on the recovery of cognitive function after immunotherapy. This study aimed to explore clinical characteristics of cognitive impairment and 1-year outcome in patients with anti-LGI1 encephalitis. Methods: The clinical data and characteristics of cognitive impairment of 21 patients with anti-LGI1 encephalitis from 2016 to 2019 in Nanjing Brain Hospital were analyzed retrospectively. At the time of onset of hospitalization and 1 year after discharge, the cognitive functions in these patients were assessed using two cognitive screening scales-Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment-Basic (MoCA-B). Results: Among the 21 patients, 13 were male and 8 were female, aged 51.10 ± 14.69 (age range 20-72) years. Nineteen patients, comprising 90.48%, had recent memory deterioration. Routine electroencephalography (EEG) results of 13 cases were abnormal. EEG results were epileptic or slow-wave activity involving the temporal lobes. Eleven cases of brain MRI were abnormal, and the focus involved the hippocampus and mediotemporal lobe. The decrease of short-term memory [recall scores: 0.57 ± 0.81 (MMSE), 0.76 ± 1.34 (MoCA-B)] is the most obvious at the time of admission. After intravenous (IV) injection of methylprednisolone and/or immunoglobulin, the clinical symptoms of the patients improved obviously. Total MMSE and MoCA-B scores of patients were significant increased after 1 year (21.19 ± 3.54 vs. 26.10 ± 3.02, P < 0.001; and 19.00 ± 4.38 vs. 25.19 ± 4.25, P < 0.001, respectively). Recall scores and orientation scores of MoCA-B were significantly improved after 1 year (0.76 ± 1.34 vs. 3.24 ± 1.48, P < 0.001; and 3.10 ± 1.26 vs. 5.00 ± 1.22, P < 0.001, respectively). However, 3/21 (14.29%) patients still have obvious short-term memory impairment (recall scores ≤ 1). Conclusion: Cognitive impairment is one of the most common manifestations of anti-LGI1 encephalitis, with the main prominent being acute or subacute short-term memory loss. Although most patients with anti-LGI1 encephalitis respond well to immunotherapy, a small number of patients still have cognitive disorders, mainly recent memory impairment, after 1 year.

Dysfunctional Dynamics of Intra- and Inter-network Connectivity in Dementia With Lewy Bodies.

Dementia with Lewy bodies (DLB) is characterized by the transient fluctuating cognition and recurrent visual hallucinations, which may be caused by disorders of the intrinsic brain network dynamics. However, little is known regarding the dynamic features of the brain network behind these symptoms in DLB. In the present study, the intra- and inter-brain network dynamics were explored on a time scale in 17 DLB and 20 healthy controls (HC) applying a sliding-window method followed by k-means clustering analysis. To further evaluate the impact of network dynamics on brain performance, the local and global efficiency of the brain network was calculated. Compared with HC, the dynamic functional connectivity variation matrix in DLB patients was represented by a mixed change of intra-network increase and inter-network decrease. DLB patients devoted more time to a negative connectivity pattern, which represents a state of functional separation. Furthermore, the local efficiency of DLB patients was significantly lower compared with HC. These observations indicate an altered dynamic variability and disorders to the time allocation of state sequences in DLB, which might result in a disturbance of the intricate brain network dynamic properties, thereby leading to a lack of integration and flexibility and an ineffective brain function. In conclusion, dynamic functional connectivity analysis could identify differences between DLB and HC, providing evidences for DLB diagnosis and contributing to the understanding of the widespread clinical features and complex treatment strategies in DLB patients.

Brain astrocytoma misdiagnosed as anti-NMDAR encephalitis: a case report.

BACKGROUND: Anti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis, which is the most common type of autoimmune encephalitis, is caused by the production of autoantibodies against NMDA receptor. Anti-NMDAR encephalitis patients present with various non-specific symptoms, such as abnormal psychiatric or behaviour, speech dysfunction, cognitive dysfunction, seizures, movement disorders, decreased level of consciousness, and central hypoventilation or autonomic dysfunction. CASE PRESENTATION: A 67-year-old man presented with new-onset focal seizures. The brain magnetic resonance imaging (MRI) plain scan and enhanced scan showed abnormal signal on the proximal midline frontoparietal junction region. Anti-NMDAR antibody was detected in cerebrospinal fluid (CSF) and serum using a commercial kit (Euroimmune, Germany) by indirect immunofluorescence testing (IIFT) according to the manufacturer's instructions for twice. Both of the test results were positive in CSF and serum. The patient was diagnosed as anti-NMDAR encephalitis and then was treated repeatedly with large dose of intravenous corticosteroids and gamma globulin. Accordingly, the refractory nature of seizures in this case may be attributed to NMDAR autoantibodies. When the patient presented at the hospital for the third time, the brain MRI revealed an increase in the size of the frontal parietal lesion and one new lesion in the left basal ganglia. The patient underwent a surgical biopsy and astrocytoma was confirmed by histopathology. CONCLUSIONS: Although the sensitivity and specificity of anti-NMDAR-IgG antibodies in CSF to diagnose anti-NMDAR encephalitis are close to 100%, it is not absolute. Anti-NMDAR antibodies were positive, which might make the diagnosis more complex. The diagnosis of atypical presentation of anti-NMDAR encephalitis requires reasonable exclusion of other disorders.

Indirubin-3'-monoxime suppresses amyloid-beta-induced apoptosis by inhibiting tau hyperphosphorylation.

Indirubin-3'-monoxime is an effective inhibitor of cyclin-dependent protein kinases, and may play an obligate role in neuronal apoptosis in Alzheimer's disease. Here, we found that indirubin-3'-monoxime improved the morphology and increased the survival rate of SH-SY5Y cells exposed to amyloid-beta 25-35 (Aß25-35), and also suppressed apoptosis by reducing tau phosphorylation at Ser199 and Thr205. Furthermore, indirubin-3'-monoxime inhibited phosphorylation of glycogen synthase kinase-3ß (GSK-3ß). Our results suggest that indirubin-3'-monoxime reduced Aß25-35-induced apoptosis by suppressing tau hyperphosphorylation via a GSK-3ß-mediated mechanism. Indirubin-3'-monoxime is a promising drug candidate for Alzheimer's disease.

Salubrinal protects against rotenone-induced SH-SY5Y cell death via ATF4-parkin pathway.

Parkinson's disease (PD) is a progressive neurodegenerative disorder, for which there are no effective disease-modifying therapies. Growing evidence from studies in human PD brain, in addition to genetic and toxicological models, indicates that endoplasmic reticulum (ER) stress is a common feature of the disease and contributes to neurodegeneration. We examine whether salubrinal, a ER stress inhibitor, can protect the rotenone-induced SH-SY5Y cell death and explore the mechanisms underlying this protection. Our results demonstrated that rotenone induced a significant ER stress response and caused cell apoptosis, which was inhibited by salubrinal. Activating transcription factor 4 (ATF4), a member of the ATF/CREB family of basic leucine zipper transcription factors, has been implicated in the pathogenesis of neurodegeneration. We showed that salubrinal increased the up-regulation of ATF4 expression. An ATF4 siRNA significantly increased the rotenone cytotoxicity and decreased the salubrinal's protection. Further, we showed that ATF4 siRNA inhibited the expression of parkin, and parkin knockdown similarly aggravated the rotenone cytotoxicity and reduced the salubrinal's protection. Additionally, the protein level of parkin was declined after treatment with rotenone, whereas this reduction was rescued by salubrinal. These findings indicate ATF4-parkin pathway plays an important role in the salubrinal-mediated neuroprotection of rotenone-induced dopaminergic cell death.

Inhibition of endoplasmic reticulum stress is involved in the neuroprotective effects of candesartan cilexitil in the rotenone rat model of Parkinson's disease.

Recent studies indicated that angiotensin II (Ang II) receptor blockers could reduce neurotoxins-induced dopaminergic (DA) cell death, but the underlying mechanisms are still unclear. Given that endoplasmic reticulum (ER) stress plays a major role in rotenone-induced neuronal apoptosis, we investigated whether candesartan cilexetil, a selective and high-affinity Ang II receptor antagonist, could protect the DA neuron via reducing ER stress in a chronic rotenone rat model for Parkinson's disease (PD). Our data showed that candesartan cilexetil could ameliorate the descent latency in catalepsy tests, and decrease rotenone-induced DA neuron apoptosis. Moreover, candesartan cilexetil has been found to play a protective role via down-regulating the expression of activating transcription factor 4 (ATF4), the CCAAT-enhancer-binding protein (C/EBP) homologous protein (CHOP), and p53 upregulated modulator of apoptosis (Puma). Thus, our experiments strongly suggest that administration of candesartan cilexetil protects DA neuron involving blocking ER stress, possibly via inhibiting activation of the ATF4-CHOP-Puma pathway, which could provide new insight into clinical therapeutics for PD.

Complete mitochondrial genome of the Spilornis cheela (Falconiformes, Accipitridae): comparison of S. cheela and Spizaetus alboniger.

Here, we sequenced the complete mitochondrial genome of Spilornis cheela (Falconiformes, Accipitridae), which is considered as endemic raptor species and listed in the second category of National Key Protected Wild Animals in China. The genome is 18,291 bp in size. Its gene arrangement pattern was identical with that of Spizaetus alboniger. We compared the mitochondrial genome of S. cheela with that of S. alboniger. Nucleotide sequence similarity between the two whole mitochondrial genomes was 84.34%, and the relatively low similarity seems to indicate that the two species are distinctly separated on the species level. The information on the mitochondrial genome comparison of the two species is discussed in detail in this paper.

Reactivation of Syk gene by AZA suppresses metastasis but not proliferation of breast cancer cells.

Spleen tyrosine kinase (Syk) is reported to be involved in the suppression of proliferation and invasion of breast cancer. Methylation-mediated Syk gene silencing is found in a subset of breast cancer. In this study, we used a DNA methyltransferase inhibitor, 5-aza-2-deoxycytidine (AZA), to restore Syk expression of breast cancer cells. Surprisingly, we found that AZA treatment could reestablish the expression of Syk, but not affect the proliferation of breast cancer cells. Moreover, tumor formation in situ by MDA-MB-435s treated with (+) or without (-) AZA in a nude mice MFP (Mammary fat pad) model did not show significant difference, too. Interestingly, pulmonary metastasis was still significantly suppressed in MDA-MB-435s(+) group (1/9 vs. 7/9). Our findings suggested Syk may be more correlated to metastasis rather than proliferation. This study implied a potential use of Syk methylation as a valuable biomarker to detect high metastatic potential cancerous lesions and the prospect of AZA to join the arsenal of drug candidates to be developed as a new reagent for management of advanced breast cancer.

The complete mitochondrial genome of Chrysolophus pictus (Galliformes: Phasianidae) and a phylogenetic analysis with related species.

The 16,678 bp mitochondrial genome of the Chrysolophus pictus has been sequenced in this paper. To determine the phylogentic position of C. pictus with related species within Phasianidae, the phylogenetic tree was reconstructed with the concatenated nucleotide dataset of the 12 heavy-strand-encoded protein genes. The phylogenetic analysis was carried out using maximum parsimony (MP) and Bayesian inference (BI) methods. MP and BI phylogenetic trees here showed similar topology and consistently suggested that C. pictus shared a close relationship with Phasianus versicolor. The results also showed that the Meleagris gallopavo possessed a basal phylogenetic position within Phasianidae, which may imply that it should be classified into the Phasianidae.

Short amyloid-beta immunogens show strong immunogenicity and avoid stimulating pro-inflammatory pathways in bone marrow-derived dendritic cells from C57BL/6J mice in vitro.

Amyloid beta peptide 1-15 (Aß1-15) and its derivatives have attracted the attention of the scientific community as candidate vaccines for Alzheimer's disease (AD) immunotherapy. Recent studies suggested that Aß1-42 modulated the immune system by inducing pro-inflammatory dendritic cells (DCs) with reduced antigen-presenting function. However, it remains elusive how Aß1-15 impacts DCs function. We therefore investigated the modulation by short Aß peptides of DCs from C57Bl/6J mice. Two new immunogens, a tandem repeat of two-lysine-linked Aß1-15 sequences with or without an addition of a RGD motif, were tested. Chemotaxis, endocytosis, antigen presenting function and producing cytokines were measured. Both peptides increased migration/endocytosis of immature DCs and MHC II molecule expression/alloreactive T cell activation in TNF-α-matured DCs. In addition, they exhibited decreased production of Th1/Th2 cytokines and pro-inflammatory cytokines. Overall, the two peptides demonstrated strong immunogenicity but did not stimulate pro-inflammatory pathways. These results support the use of short Aß immunogens in AD immunotherapy.

Angiotensin II does not directly affect Aß secretion or ß-/γ-secretase activity via activation of angiotensin II type 1 receptor.

Recent studies suggest that brain angiotensin II (Ang II), the major effector molecule of the renin-angiotensin system, is implicated in the pathogenesis of Alzheimer's disease (AD). However, it remains unknown whether activation or blockade of the angiotensin II type 1 receptor (AT1R) has an impact on the secretion of amyloid-ß (Aß), the key molecule in the pathogenesis of AD. In this study, the cell models cultured primary hippocampal neurons and human embryonic kidney 293 cells, were transfected with AT1R and amyloid precursor protein/presenilin-1 (PS1). The effects of activation/blockade of the AT1R on Aß secretion, PS1 level and ß-/γ-secretase activity were investigated in different cells. When AT1R was stimulated with Ang II at concentrations from 10nM to 1000nM, only a tendency toward increased Aß secretion and ß-/γ-secretase activity was noticed in cultured primary hippocampal neurons. However, no significant change in soluble Aß(40) or Aß(42), the level of PS1, or secretase activity was found in the cells. Similarly, when the AT1R was blocked by losartan, no significant alteration of Aß secretion, PS1 levels or secretase activity was detected. In conclusion, this in vitro study demonstrates that Ang II does not directly affect Aß secretion or secretase activity via activation of AT1R. This study is significantly meaningful for exploring the pharmacologic mechanisms of angiotensin II receptor blockers in AD.

[Application of modified paramedian forehead flap in reconstruction of nasal defect].

OBJECTIVE: To investigate the feasibility and significance of modified paramedian forehead flap for nasal defect and reconstruction. METHODS: Modified paramedian forehead flaps with forehead muscle in the pedicle were used in 2 patients with nasal reconstruction and 7 patients with nasal defects. The flaps were elevated subcutaneously with only forehead muscle in the pedicle at the supraorbital site. The degree of flap axis ranged from 90 degrees to 50 degrees. Inverted L-shape design was used for 3 cases with low hair line. RESULTS: Skin branch of supratrochlear vessel was observed running at the subcutaneous layer during the operation. 8 flaps all survived successfully with good texture and color. Partial necrosis happened in the distal end of one flap with subcutaneous pedicle, which healed through dressing. CONCLUSIONS: Modified paramedian forehead flap, which includes muscle just in the pedicle, is based on the skin branch of supratrochlear vessel. The flap is very flexible and has reliable blood supply, leaving less morbidity in donor site. It also has good texture and skin color.

[Observation on the therapeutic effects of negative-pressure wound therapy on the treatment of complicated and refractory wounds].

OBJECTIVE: To study the effects of negative-pressure wound therapy (NPWT) on the treatment of complicated and refractory wounds. METHODS: Sixty-seven patients with complicated or refractory wounds admitted to our hospital from September 2005 to November 2008 were randomly divided into NPWT group (n = 35) and conventional treatment (CT) group (n = 32). Wounds of patients in NPWT group were treated with interrupted suction under a pressure of -16.63 kPa for 24 hs, or continuous suction under a pressure of -10.64 kPa for 24 hs. Wounds of patients in CT group were covered with petrolatum gauze overlaid with isotonic saline gauze and dry gauze. Duration of treatment, times of operation, treatment cost, and the process of healing were compared between two groups. RESULTS: The duration of treatment, treatment cost and times of operation of patients in NPWT group were obviously less or fewer than those of CT group (P < 0.05). Wounds of patients in NPWT group were mainly healed by themselves (40.0%) or healed after free skin grafting (40.0%). While wounds in patients in CT group healed mainly after tissue flap transplantation (66.7%) or free skin grafting (23.3%). CONCLUSIONS: Compared with CT, NPWT can shorten the length of hospital stay, reduce operation frequency and treatment cost, and it is easier to carry out in the surgery of treating complicated and refractory wounds, which is worth generalization.

[A comparative study of the clinical effects between two kinds of negative-pressure wound therapy].

OBJECTIVE: To compare the differences of the clinical effects, side effects and treatment-related cost between two kinds of negative-pressure wound therapy (NPWT). METHODS: Forty-four inpatients with acute, subacute, and chronic wounds were divided into simplified NPWT group (A group) and conventional NPWT group (B group) according to the random number table. Wounds of patients in A group were treated with gauze + continuous suction with hospital central negative pressure (-10.64 kPa) for 24 hs; wounds of patients in B group were treated with sponge + interrupted suction with a purpose-designed suction appliance (-16.63 kPa) for 24 hs. Gross wound condition, treatment time, survival rates of skin graft and flap, changes of bacterial species on wound, treatment cost, and ratio of side effects between two groups were compared. RESULTS: There was no significant difference between A and B groups in respect of gross wound condition, treatment time [A group (29 +/- 12) d, B group (26 +/- 13) d, P > 0.05], changes of bacterial species, survival rates of skin graft [A group (98 +/- 4)%, B group (98 +/- 4)%, P > 0.05] and flap (A group 98%, B group 100%, P > 0.05). Treatment cost of A group yen(374 +/- 134) was obviously lower than that of B group yen(9825 +/- 4956) (P < 0. 01), while more side effects were observed in A group (33.3%) than that in B group (5.0%) (P < 0.05). CONCLUSIONS: Both simplified NPWT and NPWT with purpose-designed appliance can effectively improve wound healing. The simplified method may cause many side effects and has a potential risk of inciting nosocomial infection, but it can be conveniently employed with a low cost. In contrast, the cost of using purpose-designed appliance should be cut down to meet the aim of generalization.

Plasma resistin levels and single-nucleotide polymorphisms in resistin gene 5' flanking region in patients with stroke.

OBJECTIVE: To analyze the role of resistin in insulin resistance (IR) through investigating the variation of plasma resistin levels and single-nucleotide polymorphisms (SNPs) in resistin gene 5' flanking region in stroke patients. METHODS: In 103 atherothrombotic cerebral infarction (ACI) patients, 85 lacunar infarction (LI) patients, 70 intracerebral hemorrhage (ICH) patients, and 86 healthy controls, plasma resistin and insulin levels were measured by ELISA, SNPs in resistin gene 5' flanking region were detected by PCR and direct DNA sequencing. The subjects' body height and weight, the body mass index, quantitative insulin sensitivity check index (QUICKI), blood pressure, and the concentration of fasting plasma glucose, triglyceride, total cholesterol, creatinine, low-density lipoprotein, and high-density lipoprotein were also determined. RESULTS: QUICKI was significantly lower in the ACI and ICH patients (0.316 +/- 0.037 and 0.309 +/- 0.032, respectively) than that in the controls (0.342 +/- 0.043, P < 0.001), while plasma resistin level was significantly higher in the ACI and ICH patients (6.36 +/- 3.79 and 7.15 +/- 4.27 ng/mL, respectively) than that in the controls (5.28 +/- 2.56 ng/mL, P < 0.05), but such difference was not observed in the LI patients compared with controls. There was a statistically negative correlation between plasma resistin level with QUICKI (r = -0.228, P < 0.001). The distributions of allele and genotype frequencies of resistin gene - 420C > G and - 537A > C SNPs were not significantly different among the different groups, and those SNPs were not correlated with other clinical and biochemical parameters. CONCLUSIONS: Plasma resistin is associated with stroke by participating in the development of IR. The SNPs in resistin gene 5' flanking region has no impact on the plasma resistin level.

[Determination of sodium phenytoin in plasma by high performance capillary zone electrophoresis].

A method to determine sodium phenytoin in plasma by high performance capillary zone electrophoresis (CZE) has been established. CZE was performed in 25 mmol/L phosphate buffer solution (pH 12) at 20 degrees C. The capillary column size was 75 microns i.d. x 30 cm (effective length). Sodium phenytoin was quantified with UV detector at 200 nm. The plasma was extracted by ether after plasma was processed with proteinase K for 3 h at 55 degrees C. Then the extract was evaporated to dryness. The residue was reconstituted in 1 mL of running buffer. The average recovery was higher than 95%. The precisions of intra-day and inter-day were 3.1% and 4.7% respectively. The detection limit of sodium phenytoin was 0.6 mg/L.