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Background: On diagnosis of human immunodeficiency virus (HIV) infection, a person may have been infected already for many years. This study aimed to estimate the duration of HIV infection at the time of diagnosis. Methods: Newly diagnosed HIV cases in Dehong, China, from 2008 to 2015 were studied. Duration of infection at the time of diagnosis was calculated using the first CD4 cell count result after diagnosis and a CD4 depletion model of disease progression. Multiple linear regression analysis was used to investigate the associated risk factors. Results: A total of 5867 new HIV cases were enrolled. Overall, mean duration of infection was 6.3 years (95% confidence interval [CI]: 6.2, 6.5). After adjusting for confounding, significantly shorter durations of infection were observed among participants who were female (beta: −0.37, 95% CI: −0.64, −0.09), Dai ethnicity (beta: −0.28, 95% CI: −0.57, 0.01), and infected through injecting drug use (beta: −1.82, 95% CI: −2.25, −1.39). Compared to the hospital setting, durations were shorter for those diagnosed in any other settings, and compared to 2008, durations were shorter for those diagnosed all years after 2010. Results: A total of 5867 new HIV cases were enrolled. Overall, mean duration of infection was 6.3 years (95% confidence interval [CI]: 6.2, 6.5). After adjusting for confounding, significantly shorter durations of infection were observed among participants who were female (beta: −0.37, 95% CI: −0.64, −0.09), Dai ethnicity (beta: −0.28, 95% CI: −0.57, 0.01), and infected through injecting drug use (beta: −1.82, 95% CI: −2.25, −1.39). Compared to the hospital setting, durations were shorter for those diagnosed in any other settings, and compared to 2008, durations were shorter for those diagnosed all years after 2010. Conclusion: Although the reduction in duration of infection at the time of diagnosis observed in Dehong was significant, it may not have had a meaningful impact.

Background: Standard automated perimetry does not sufficiently detect early open-angle glaucoma (OAG) in the clinic. New visual function tests for early glaucoma damage are therefore needed. The present study evaluated whether an isolated-check visual evoked potential (icVEP) could be used to detect visual function abnormalities in early-stage OAG and to explore potential related factors. Methods: This was a cross-sectional study. Thirty-seven OAG patients with early-stage visual field loss (mean deviation ≥ −6.00 dB) detected by the Humphrey Field Analyzer (30-2 SITA program) and 26 controls were included in this study. Optical coherence tomography (OCT) was used to detect retinal nerve fiber layer (RNFL) defects. The icVEP preferentially evaluates the magnocellular-ON pathway. VEPs were recorded and signal-to-noise ratios (SNRs) were derived based on multivariate analysis. Eyes that yielded an SNR ≤1 were considered abnormal. Receiver operating characteristic (ROC) curve analysis was used to estimate the accuracy of group classification. Correlations between SNRs and related factors were analyzed. Results: Based on an SNR criterion of 1, the icVEP had a sensitivity of 62.2% and a specificity of 92.3% for diagnosing early-stage OAG with 74.6% classification accuracy. The ROC curve analysis, however, suggested that an SNR criterion of 0.93 would produce the highest classification accuracy (77.3%). Both RNFL thinning in the temporal superior quadrant on OCT and number of abnormal test points in the central 11° visual field (pattern deviation, P < 0.5%) significantly correlated with the SNR (P < 0.05). Conclusions: The icVEP detected visual function abnormalities in approximately 3/5 of eyes with early-stage OAG with greater than 90% specificity. SNR correlated with both a decrease in RNFL thickness and severity of central visual field loss. Key words: Cross-Sectional Study; Isolated-Check; Open-Angle Glaucoma; Signal-To-Noise Ratios; Visual Evoked Potential

Background: Patients on hemodialysis have a high-mortality risk. This study analyzed factors associated with death in patients on maintenance hemodialysis (MHD). While some studies used baseline data of MHD patients, this study used the most recent data obtained from patients just prior to either a primary endpoint or the end of the study period to find the characteristics of patients preceding death. Methods: Participants were selected from 16 blood purification centers in China from January 2012 to December 2014. Patients’ data were collected retrospectively. Based on survival status, the participants were divided into two groups: survival group and the death group. Logistic regression analysis was performed to determine factors associated with all-cause mortality. Results: In total, 4104 patients (57.58% male, median age 59 years) were included. Compared with the survival group, the death group had more men and more patients with diabetic nephropathy (DN) and hypertensive nephropathy. The patients preceding death also had lower levels of diastolic blood pressure, hemoglobin, serum albumin, serum calcium, serum phosphate, Kt/V, and higher age. Multivariate analysis revealed that male sex (odd ratio [OR]: 1.437, 95% confidence interval [CI]: 1.094–1.886), age (OR: 1.046, 95% CI: 1.036–1.057), and presence of DN (OR: 1.837, 95% CI: 1.322–2.552) were the risk factors associated with mortality. High serum calcium (OR: 0.585, 95% CI: 0.346–0.989), hemoglobin (OR: 0.974, 95% CI: 0.967–0.981), albumin (OR: 0.939, 95% CI: 0.915–0.963) levels, and dialysis with noncuffed catheter (OR: 0.165, 95% CI: 0.070–0.386) were protective factors based on a multivariate analysis. Conclusions: Hemodialysis patients preceding death had lower hemoglobin, albumin, and serum calcium levels. Multivariate analysis showed that male sex, age, DN, low hemoglobin, low albumin, and low serum calcium were associated with death in hemodialysis patients. Key words: Hemodialysis; Mortality; Risk Factors

BACKGROUND Reading Chinese, a kind of ideogram, relies more on visual cognition. The visuospatial cognitive deficit of Chinese dyslexia is an interesting topic that has received much attention. The purpose of current research was to explore the visuopatial cognitive characteristics of Chinese dyslexic children by studying their eye movements via a picture searching test. METHODS According to the diagnostic criteria defined by ICD-10, twenty-eight dyslexic children (mean age (10.12 +/- 1.42) years) were enrolled from the Clinic of Children Behavioral Disorder in the third affiliated hospital of Sun Yat-sen University. And 28 normally reading children (mean age (10.06 +/- 1.29) years), 1:1 matched by age, sex, grade and family condition were chosen from an elementary school in Guangzhou as a control group. Four groups of pictures (cock, accident, canyon, meditate) from Picture Vocabulary Test were chosen as eye movement experiment targets. All the subjects carried out the picture searching task and their eye movement data were recorded by an Eyelink II High-Speed Eye Tracker. The duration time, average fixation duration, average saccade amplitude, fixation counts and saccade counts were compared between the two groups of children. RESULTS The dyslexic children had longer total fixation duration and average fixation duration (F = 7.711, P < 0.01; F = 4.520, P < 0.05), more fixation counts and saccade counts (F = 7.498, P < 0.01; F = 11.040, P < 0.01), and a smaller average saccade amplitude (F = 29.743, P < 0.01) compared with controls. But their performance in the picture vocabulary test was the same as those of the control group. The eye movement indexes were affected by the difficulty of the pictures and words, all eye movement indexes, except saccade amplitude, had a significant difference within groups (P < 0.05). CONCLUSIONS Chinese dyslexic children have abnormal eye movements in picture searching, applying slow fixations, more fixations and small and frequent saccades. Their abnormal eye movement mode reflects the poor ability and strategy of visual information processing.

Oculocutaneous albinism (OCA) is a heterogeneous and autosomal recessive disorder in all populations worldwide. The mutational spectra of OCA are population-specific. Some OCA patients carry mutations from different OCA genes. In this study, we investigated the frequency of digenic mutations in Chinese OCA patients.Genomic DNAs were extracted from the blood samples of 184 clinically diagnosed OCA patients and 120 unaffected subjects. The amplified DNA segments of the exons and exon-intron boundaries were screened for mutations of TYR, OCA2, TYRP1, SLC45A2, and HPS1 by direct sequencing. To exclude the previously unidentified alleles from polymorphisms, samples from 120 unaffected controls were sequenced for the same regions of variations.In all 184 patients, 134 had two pathologic mutations on one locus. Eleven cases had no apparent pathologic mutations in any of the genes studied. Among the remaining 39 patients who had only one pathologic mutation, five patients (2.7% in total) were found to carry the mutational alleles on a second locus in TYR, OCA2 or SLC45A2. Of the five digenic OCA patients, four patients were clinically diagnosed as OCA2 and one patient as OCA1. A previous unidentified allele p.G188D in SLC45A2 was identified, which was not present in the 120 unaffected controls.The identification of the digenic OCA patients suggests the synergistic roles among TYR, OCA2 and SLC45A2 during melanin biosynthesis, which may cause OCA under digenic mutations. This information will be useful for gene diagnosis and genetic counseling of OCA in China.

Paroxysmal kinesigenic dyskinesia (PKD) is characterized by recurrent brief episodes of chorea and dystonia induced by sudden movement. Whether the central nervous system is hyper- or hypoexcitable in PKD remains undetermined. The aim of our study was to compare the somatosensory evoked potential (SEP) recovery cycle, a marker of somatosensory system excitability, in PKD patients and controls.Twenty-four PKD patients (mean age of (20.0±5.3) years; 21 males, 3 females) and 18 control age-matched subjects (mean age of (22.0±5.0) years; 17 males, 1 female) were studied. The stimuli were delivered to the median nerve in the affected dominant arm in patients and in the dominant arm in controls. The change in SEP amplitude was measured after paired electrical stimulation at interstimulus intervals (ISIs) of 5, 20, and 40 ms. The SEPs evoked by S2 (test stimulus) were calculated by subtracting the response to S1 (the conditioning stimulus) from the response to a pair of stimuli (S1+S2), and their amplitudes were compared with those of the control response (S1) at each ISI. Analysis of variance (ANOVA) or equivalent was used for non-parametric data.In patients, the P27 amplitude after the single stimulus (S1) was significantly larger than that after the control stimulus. The (S2/S1)×100 ratio for P14 and N30 SEPs did not differ significantly between PKD patients and normal subjects at ISI of 5 ms but were significantly higher in patients at ISIs of 20 and 40 ms (P0.05).Somatosensory system disinhibition takes place in PKD. The finding of reduced suppression of different SEPs, each thought to have a different origin, suggests an abnormality of intracortical and subcortical inhibitory circuits.

The mutation of the tyrosinase (TYR) gene results in oculocutaneous albinism type 1 (OCA1), an autosomal recessive genetic disorder. OCA1 is the most common type of OCA in the Chinese population. Hence, the TYR gene was tested in this study. We also delineated the genetic analysis of OCA1 in a Chinese family.Genomic DNA was isolated from the blood leukocytes of a proband and his family. Mutational analysis at the TYR locus by DNA sequencing was used to screen five exons, including the intron/exon junctions. A pedigree chart was drawn and the fundus of the eyes of the proband was also examined.A novel missense mutation p.I151S on exon 1, and homozygous TYR mutant alleles were identified in the proband. None of the mutants was identified among the 100 normal control subjects. Genetic analysis of the proband's wife showed normal alleles in the TYR gene. Thus, the fetus was predicated a carrier of OCA1 with a normal appearance.This study provided new information about a novel mutation, p.I151S, in the TYR gene in a Chinese family with OCA1. Further investigation of the proband would be helpful to determine the effects of this mutation on TYR activity.

Recent studies have discovered that nuclear translocation of nerve growth factor (NGF) and its receptor fragments function differently from the traditional model. This study aimed to uncover the nuclear expression of NGF in astrocytoma and its biological significance.Ninety-four paraffin-embedded astrocytoma specimens were subjected to immunohistochemical (IHC) and hemotoxylineosin (HE) staining. Preoperative cerebrospinal fluid (CSF) specimens and intraoperative snap-frozen astrocytoma tissues were assayed for NGF expression by ELISA and Western blotting. The outcome of patients who contributed samples was tracked. Each ten tissue samples from patients with traumatic brain injury who had received decompression surgery and CSF samples from patients undergoing spinal anesthesia but with no history of nervous system disease were taken as control.NGF-positive immunoreactive products were distributed in both the cytoplasm and nucleus of astrocytoma, but were only located in the cytoplasm of traumatic brain injury (TBI) tissue. NGF nuclear-positive rate (NPR) of grades III - IV astrocytomas (70.0%) was higher than that of grades I - II astrocytoma (28.6%, P0.05). NGF-NP expression positively correlated with the NGF concentration in cerebrospinal fluid (CSF) (r = 0.755, P0.01). Kaplan-Meier survival analysis indicated that the median survival time was 25 months for NGF-NP astrocytoma grade I - II patients and 42 months in NGF nuclear negative (NGF-NN) astrocytoma grade I - II patients (P0.05). In astrocytoma III - IV patients, the median survival was 7 months for NGF-NP patients and 24 months for NGF-NN patients (P0.01). Two types of NGF with molecular weights of 13 and 36 kDa were present in astrocytoma, but only the 36 kDa NGF was found in the CSF. NGF expression elevated as the malignancy increased.NGF-NP expression and NGF level in CSF were significant prognostic factors in astrocytoma patients. Because of the easy access of CSF, it may be developed as an index for early diagnosis and surveillance of astrocytoma.

Implantation of tissue-engineered scaffolds is one of the most promising therapeutic strategies for inducing nerve regenerations following spinal cord injuries. In this paper, we report a novel bioengineered hybrid scaffold comprised of three major extracellular matrix (ECM) proteins.ECM-scaffolds (ECM-S) were prepared by gelling fibrinogen, fibronectin and laminin using fresh rat plasma. Olfactory ensheathing cells (OECs) were isolated from fresh rat olfactory mucosa, purified under differential adhesion, and assessed by immunofluorescent staining. OECs were seeded onto ECM-S and cultured. The effects of the scaffolds on the seeded cells were detected using the immunofluorescent staining, Western blotting, scanning electron microscopy and transmission electron microscopy.Tissue-engineered ECM-S could be easily molded into mat-like or cylindrical shapes and gelled by addition of fresh plasma. Observations by electron microscopy show that the ECM-S forms a stable three-dimensional porous network. Studies on the effects of the ECM-S on the biological behaviors of OECs in vitro indicate that the scaffold can promote OEC adhesion, proliferation and process extensions. Additionally, OECs seeded on the scaffold maintained the expression of nerve growth factor, matrix metalloproteinase-3 and matrix metalloproteinase-9.We developed a biosynthetic hybrid gel which could be used as a scaffold for OEC transplantation; this gel can promote nerve regeneration following spinal cord injuries.

Background Corneal neovascular leakage can lead to edema and secondary scarring. Previous studies have shown that pericytes play a key role in maturation of angiogenesis. The present studies investigate the relationship between vascular permeability and pericyte coverage of endothelial cells in rat corneal neovascular induced by alkali burns. Methods Corneal neovascular vessels induced by alkali burns was performed in Sprague-Dawley rats. Corneas were excised on 1, 2, 3, 5, 7 and 10 days after cauterization. The vascular permeability rate was measured by the Evans blue method. The microvessel pericyte coverage index (MPI) was applied to quantify the pericyte coverage through double immunofluorescent staining of frozen sections of corneas with CD31 as the endothelial and alpha-smooth muscle actin (alpha-SMA) as the pericyte markers. The correlation between permeability rate and MPI was analyzed. Pericyte coverage was confirmed ultrastructually using transmission electron microscopy. Results The vascular permeability rate was (1.14 +/- 0.17), (0.24 +/- 0.08), (0.29 +/- 0.16), (0.14 +/- 0.10), (0.09 +/- 0.06) and (0.05 +/- 0.04) microg x ml(-1) x mm(-2) respectively on 1, 2, 3, 5, 7 and 10 days after cauterization. The MPI was 0, 16.07%, 11.95%, 43.84%, 73.97% and 86.21% respectively at the above mentioned time points. The correlation coefficient between MPI and the permeability rate was -0.943 (P = 0.005). Conclusions Pericyte recruitment was significantly correlated with the permeability of corneal neovascularization induced by alkali burns in rats. Therapeutic strategies aiming at anti-leakage should be most effective if they promote pericytes proliferation in the course of corneal neovascularization.

5-dihydroxyanthraquinone-2-carboxylic acid (rhein) inhibits oxidoreduction induced by reducing nicotingamide adenine dinucleotide in the mitochondria and reducing reactive oxygen species, it also suppresses lipid peroxidation in rat brain homogenates. This study was to assess the effects of anthraquinone derivatives, rhein on synaptic transmission in the rat hippocampal CA1 pyramidal cell layer by intracellular recording.The excitatory postsynaptic potential (EPSP) evoked by stimulation of the Schaffer collaterals in the presence of bicuculline (15 micromol/L) was depressed by application of rhein (0.3 - 30 micromol/L). The amplitude of the EPSP was restored within 20 minutes after removal of rhein from the supernatant. At a concentration of 30 micromol/L, rhein reduced the amplitude of the EPSP to 42% +/- 3.7% (n = 24) of the control. Subsequently, wavelet spectral entropy was used to analyze the EPSP.A strong positive correlation was observed between the wavelet spectral entropy and other parameters such as amplitude, slope of rising phase and slope of descending phase of the EPSP. The paired-pulse facilitation (PPF) of the EPSP was significantly increased by rhein (30 micromol/L). The inhibitory postsynaptic potential (IPSP) recorded in the presence of CNQX (20 micromol/L) and APV (40 micromol/L) is not altered by rhein (30 micromol/L).Rhein (30 micromol/L) can decrease the frequency but not the amplitude of the miniature EPSP (mEPSP). It is suggested that rhein inhibits excitatory synaptic transmission by decreasing the release of glutamate in rat hippocampal CA1 pyramidal neurons.

The activation of extracellular signal-regulated kinase1/2 (ERK1/2) has been shown to be important signaling pathway in the ischemic preconditioning (IPC) response. Recently, some studies suggest a key role for the mitochondrial ATP-sensitive potassium channel (mKATP) as both a trigger and an end effector of acute and delayed protection of IPC. Hence, this study was undertaken to elucidate the relationship between mKATP and ERK1/2 in the delayed protection mechanism of anoxic preconditioning (APC).An APC model was established using cultured neonatal rat cardiomyocytes. Pharmacological agents [diazoxide, 5-hydroxydecanoate (5-HD), 2-mercaptopropionylglycine (MPG), and PD98059] were used to modulate mKATP and ERK1/2 activation. Cellular injury was evaluated by measuring cellular superoxide dismutase (SOD) activity, cell viability, and lactate dehydrogenase (LDH) release. The generation of cellular reactive oxygen species (ROS) and the activation of ERK1/2 were determined at different time points starting from the beginning of preconditioning with anoxia or diazoxide (an mKATP opener).Cell viability and SOD activity in the APC [(81.9 +/- 11.4)%, (13.6 +/- 3.7) U/L] and diazoxide [(79.2 +/- 12.4)%, (16.5 +/- 4.6) U/L] groups were significantly higher than in the anoxia/reoxygenation (A/R) [(42.2 +/- 7.3)%, (8.8 +/- 2.8) U/L] group (all P0.01). LDH activity in the APC group [(101.9 +/- 18.9) U/L] and diazoxide group [(97.5 +/- 17.7) U/L] was significantly lower than in the A/R group [(250.5 +/- 43.6) U/L] (all P0.01). Both APC and diazoxide simultaneously facilitated intracellular ROS generation and rapid ERK1/2 activation. But the effects of APC and diazoxide were remarkedly attenuated by 5-HP (an mKATP blocker) and by MPG (a free radical scavenger). In addition, the ERK1/2 inhibitor PD98059 also abolished the cellular protective effects induced by diazoxide.mKATP may mediate ERK1/2 activation during anoxia preconditioning by generating ROS, which then triggers the delayed protection of APC in rat cardiomyocytes.