Resetting transcription factor control circuitry toward ground-state pluripotency in human.

Current human pluripotent stem cells lack the transcription factor circuitry that governs the ground state of mouse embryonic stem cells (ESC). Here, we report that short-term expression of two components, NANOG and KLF2, is sufficient to ignite other elements of the network and reset the human pluripotent state. Inhibition of ERK and protein kinase C sustains a transgene-independent rewired state. Reset cells self-renew continuously without ERK signaling, are phenotypically stable, and are karyotypically intact. They differentiate in vitro and form teratomas in vivo. Metabolism is reprogrammed with activation of mitochondrial respiration as in ESC. DNA methylation is dramatically reduced and transcriptome state is globally realigned across multiple cell lines. Depletion of ground-state transcription factors, TFCP2L1 or KLF4, has marginal impact on conventional human pluripotent stem cells but collapses the reset state. These findings demonstrate feasibility of installing and propagating functional control circuitry for ground-state pluripotency in human cells.

Suppression of YAP safeguards human naïve pluripotency.

Propagation of human naïve pluripotent stem cells (nPSCs) relies on the inhibition of MEK/ERK signalling. However, MEK/ERK inhibition also promotes differentiation into trophectoderm (TE). Therefore, robust self-renewal requires suppression of TE fate. Tankyrase inhibition using XAV939 has been shown to stabilise human nPSCs and is implicated in TE suppression. Here, we dissect the mechanism of this effect. Tankyrase inhibition is known to block canonical Wnt/ß-catenin signalling. However, we show that nPSCs depleted of ß-catenin remain dependent on XAV939. Rather than inhibiting Wnt, we found that XAV939 prevents TE induction by reducing activation of YAP, a co-factor of TE-inducing TEAD transcription factors. Tankyrase inhibition stabilises angiomotin, which limits nuclear accumulation of YAP. Upon deletion of angiomotin-family members AMOT and AMOTL2, nuclear YAP increases and XAV939 fails to prevent TE induction. Expression of constitutively active YAP similarly precipitates TE differentiation. Conversely, nPSCs lacking YAP1 or its paralog TAZ (WWTR1) resist TE differentiation and self-renewal efficiently without XAV939. These findings explain the distinct requirement for tankyrase inhibition in human but not in mouse nPSCs and highlight the pivotal role of YAP activity in human naïve pluripotency and TE differentiation. This article has an associated 'The people behind the papers' interview.

Deciphering adipose development: Function, differentiation and regulation.

The overdevelopment of adipose tissues, accompanied by excess lipid accumulation and energy storage, leads to adipose deposition and obesity. With the increasing incidence of obesity in recent years, obesity is becoming a major risk factor for human health, causing various relevant diseases (including hypertension, diabetes, osteoarthritis and cancers). Therefore, it is of significance to antagonize obesity to reduce the risk of obesity-related diseases. Excess lipid accumulation in adipose tissues is mediated by adipocyte hypertrophy (expansion of pre-existing adipocytes) or hyperplasia (increase of newly-formed adipocytes). It is necessary to prevent excessive accumulation of adipose tissues by controlling adipose development. Adipogenesis is exquisitely regulated by many factors in vivo and in vitro, including hormones, cytokines, gender and dietary components. The present review has concluded a comprehensive understanding of adipose development including its origin, classification, distribution, function, differentiation and molecular mechanisms underlying adipogenesis, which may provide potential therapeutic strategies for harnessing obesity without impairing adipose tissue function.

General Separation of Carbon Dots by Polyamide Chromatography.

Carbon dot (C-dot) separation/purification is not only a fundamental chemical issue but also an essential precondition for revealing C-dots' true nature. To date, adequate separation of C-dots has remained an open question due to the lack of an appropriate fine separation system. Herein, we discover and reveal that polyamide chromatography can provide versatile and powerful performances for C-dot separation. By a joint study of experiments and all-atom molecular dynamics simulations, we demonstrate that multiple interaction forces, including electrostatic repulsion/attraction, hydrogen bond, and van der Waals effects, exist simultaneously among the stationary phase, mobile phase, and the separated C-dots. Furthermore, the magnitude of these forces is dependent on the surface chemistry of the separated C-dots and the nature of the used mobile phases, providing a theoretical basis and experimental operability for C-dot separation. So, the proposed system possesses the capacity for adequately separating hydrophilic, amphiphilic, and lipophilic C-dots. The polyamide chromatography, due to its versatile and powerful separation performances, not only provides more thorough separation effects but also helps to correct our false perceptions from inadequate purified C-dots.

Protective Effect of CD137 Deficiency against Post-infarction Cardiac Fibrosis and Adverse Cardiac Remodeling via ERK1/2 Signaling Pathways.

Myocardial fibrosis, a common complication of myocardial infarction (MI), is characterized by excessive collagen deposition and can result in impaired cardiac function. The specific role of CD137 in the development of post-MI myocardial fibrosis remains unclear. Thus, this study aimed to elucidate the effects of CD137 signaling using CD137 knockout mice and in vitro experiments. CD137 expression levels progressively increased in the heart following MI, particularly in myofibroblast, which play a key role in fibrosis. Remarkably, CD137 knockout mice exhibited improved cardiac function and reduced fibrosis compared to wild-type mice at day 28 post-MI. The use of Masson's trichrome and picrosirius red staining demonstrated a reduction in the infarct area and collagen volume fraction in CD137 knockout mice. Furthermore, the expression of alpha-smooth muscle actin (α-SMA) and collagen I, key markers of fibrosis, was decreased in heart tissues lacking CD137. In vitro experiments supported these findings, as CD137 depletion attenuated cardiac fibroblast differentiation, and migration, and collagen I synthesis. Additionally, the administration of CD137L recombinant protein further promoted α-SMA expression and collagen I synthesis, suggesting a pro-fibrotic effect. Notably, the application of an inhibitor targeting the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway attenuated the pro-fibrotic effects of CD137L. To conclude, this study provides evidence that CD137 plays a significant role in promoting myocardial fibrosis after MI. Inhibition of CD137 signaling pathways may hold therapeutic potential for mitigating pathological cardiac remodeling and improving post-MI cardiac function.

Nanog is the gateway to the pluripotent ground state.

Pluripotency is generated naturally during mammalian development through formation of the epiblast, founder tissue of the embryo proper. Pluripotency can be recreated by somatic cell reprogramming. Here we present evidence that the homeodomain protein Nanog mediates acquisition of both embryonic and induced pluripotency. Production of pluripotent hybrids by cell fusion is promoted by and dependent on Nanog. In transcription factor-induced molecular reprogramming, Nanog is initially dispensable but becomes essential for dedifferentiated intermediates to transit to ground state pluripotency. In the embryo, Nanog specifically demarcates the nascent epiblast, coincident with the domain of X chromosome reprogramming. Without Nanog, pluripotency does not develop, and the inner cell mass is trapped in a pre-pluripotent, indeterminate state that is ultimately nonviable. These findings suggest that Nanog choreographs synthesis of the naive epiblast ground state in the embryo and that this function is recapitulated in the culmination of somatic cell reprogramming.

Liver Injury Traceability: Spatiotemporally Monitoring Oxidative Stress Processes by Unit-Emitting Carbon Dots.

Exploring the etiology of liver injury is critical to fundamental science and precise treatment, which has not yet been achieved by molecule imaging techniques. Herein, we manage to conquer this challenge by spatiotemporally monitoring oxidative stress processes using the proposed unit-emitting carbon dots (UE-C-dots) as fluorescent probes. We discover and reveal that the UE-C-dots can specifically determine hypochlorous acid (HClO) molecules, one of the important reactive oxygen/nitrogen species (ROS/RNS) in liver injury, by an excited state oxidation mechanism. Other ROS/RNS do not interfere with the assay even if their concentrations are 1000 times higher than that of HClO due to the lowest unoccupied molecular orbital level mismatch. Real-time tomographic imaging demonstrates that different stimuli cause distinctly different HClO bursts in both temporal and spatial dimensionalities. Therefore, the measurement and analysis of temporal information substantially extend our understanding on the relationships of hepatic oxidative stress and corresponding physiological/pathological behaviors.

Association between atherogenic index of plasma and periodontitis among U.S. adults.

BACKGROUND: Serum lipids have been proven to influence periodontitis. The atherogenic index of plasma (AIP) is an important marker of lipid levels. The purpose of this study was to investigate the association between periodontitis and AIP in adults. METHODS: The study included participants from the 2009-2014 National Health and Nutrition Examination Survey who received a complete periodontal exam and a complete record of AIP. AIP was calculated as log10 (triglycerides/high-density lipoprotein cholesterol). Periodontitis can be classified into four categories based on attachment loss and probing depth (no periodontitis, moderate periodontitis, mild periodontitis, and severe periodontitis). Multivariable logistic regression after adjusting and hierarchical analysis were conducted to investigate the relationship between periodontitis and AIP in adults. RESULTS: The final sample included 4,371 participants, representing approximately 60 million people in the United States. Periodontitis among the AIP groups (quartile, Q1-Q4) was statistically significant (P < 0.05). Univariate analysis showed that AIP was associated with the incidence of periodontitis (P < 0.05), but not with the severity of periodontitis (P > 0.05) in participants. Multifactorial logistic regression analysis showed no correlation between the incidence of periodontitis and AIP among all participants (the trend P-value = 0.341), but a significant association with AIP in the non-smoking participants (the trend P-value = 0.031). CONCLUSION: There was a significant correlation between periodontitis and AIP in the non-smoking population.

Calsyntenin-1 Promotes Doxorubicin-induced Dilated Cardiomyopathy in Rats.

PURPOSE: Doxorubicin is an important cancer chemotherapeutic agent with severe cardiotoxic effects that eventually lead to dilated cardiomyopathy (DCM). Calsyntenin-1(CLSTN1) plays a critical role in the nervous system, but its relevance in cardiovascular diseases is unknown. We investigated the significance of CLSTN1 in doxorubicin-induced DCM. METHODS: CLSTN1 expression in doxorubicin-induced DCM rats and H9c2 cells was determined using western blotting. To further explore the functions of CLSTN1, a cardiac-specific CLSTN1 overexpression rat model was constructed. The rats were subjected to analysis using echocardiographic, hemodynamic, and electrocardiographic parameters. Potential downstream molecules in CLSTN1 overexpression heart tissue were investigated using proteomics and western blotting. Finally, a knockdown of CLSTN1 was constructed to investigate the rescue function on doxorubicin-induced cell toxicity. RESULTS: CLSTN1 protein expression increased drastically in doxorubicin-induced DCM rats and H9c2 cells. Under doxorubicin treatment, CLSTN1 protein-specific overexpression in the heart muscle promoted cardiac chamber enlargement and heart failure, while the knockdown of CLSTN1 reduced doxorubicin-induced cardiomyocyte toxicity in vitro. At the mechanistic level, overexpression of CLSTN1 downregulated SERCA2 expression and increased the phosphorylation levels of PI3K-Akt and CaMK2. CONCLUSION: Our findings demonstrated that CLSTN1 promotes the pathogenesis of doxorubicin-induced DCM. CLSTN1 could be a therapeutic target to prevent the development of doxorubicin-induced DCM.

Perk heterozygosity ameliorates chronic hypoxia-induced pulmonary hypertension and right ventricular hypertrophy in male rats.

BACKGROUND: Pulmonary hypertension (PH) is a rare and deadly disease characterized by remodeling of the pulmonary vasculature and increased pulmonary artery pressure. hypobaric pulmonary hypertension (HPH) is clinically classified as group 4 of pulmonary hypertension and has a poor prognosis . Previous reports showed that HPH was associated with increased endoplasmic reticulum (ER) stress. The protein kinase R-like endoplasmic reticulum kinase (PERK) is an ER-associated stress protein. However, to date, its physiological effects on HPH and RVF development remains unknown. This study aimed to assess PERK's role in HPH and RV function using in vivo experimental model. METHODS: Perk-knockout male Sprague-Dawley rats were generated and were housed in either a hypobaric chamber or in a normoxic environment. After stimulation for 4 weeks, the hemodynamic parameters of the rats were measured. The heart and lungs were harvested for pathological observation. Blood was collected for the detection of inflammatory indexes. The right ventricle tissue was collected to assess phosphorylated-AKT, ROCK1, ET1, and MMP2 protein expression. RESULTS: WE FIRSTLY GENERATED PERK+/− RATS,: Under normal conditions, Perk+/- rats showed no changes in mPAP(mean pulmonary artery pressure), RVHI(Right ventricular hypertrophy index), cardiomyocyte size and interstitial fibrosis, and pulmonary vascular remodeling. However, in response to chronic hypoxia, Perk+/- rats exhibited decreased in mPAP, RVHI, ventricular fibrosis, and lung remodeling compared to wild-type rats. Perk+/- rats also showed lower expression of phosphor-AKT, ROCK1, ET1, and MMP2 protein in response to chronic hypoxia. CONCLUSIONS: These findings suggest that Perk heterozygosity protects against HPH and Perk may be a suitable target for treating HPH.

Iron Source and Medium pH Affect Nutrient Uptake and Pigment Content in Petunia hybrida 'Madness Red' Cultured In Vitro.

Deficiency or excess of iron (Fe) and improper medium pH will inhibit the growth and development of plants, reduce the transfer and utilization of energy from the root to the leaf, and affect the utilization efficiency of inorganic nutrients. The most common symptom of Fe deficiency in plants is chlorosis of the young leaves. In this study, the effects of the iron source, in combination with the medium pH, on plant growth and development, plant pigment synthesis, and nutrient uptake in a model plant Petunia hybrida cultured in vitro were investigated. Iron sulfate (FeSO4·7H2O) or iron chelated with ethylenediaminetetraacetic acid (Fe-EDTA) were supplemented to the MNS (a multipurpose nutrient solution) medium at a concentration of 2.78 mg·L-1 Fe, and the treatment without any Fe was used as the control. The pH of the agar-solidified medium was adjusted to either 4.70, 5.70, or 6.70 before autoclaving. The experiment was carried out in an environmentally controlled culture room with a temperature of 24 °C with 100 µmol·m-2·s-1 photosynthetic photon flux density (PPFD) supplied by white light emitting diodes (LEDs) during a photoperiod of 16 h a day, 18 °C for 8 h a day in the dark, and 70% relative humidity. Regardless of the Fe source including the control, the greatest number of leaves was observed at pH 4.70. However, the greatest lengths of the leaf and root were observed in the treatment with Fe-EDTA combined with pH 5.70. The contents of the chlorophyll, carotenoid, and anthocyanin decreased with increasing medium pH, and contents of these plant pigments were positively correlated with the leaf color. The highest soluble protein content and activities of APX and CAT were observed in the Fe-EDTA under pH 5.70. However, the GPX activity was the highest in the control under pH 4.70. In addition, the highest contents of ammonium (NH4+) and nitrate (NO3-) were measured in the FeSO4-4.7 and EDTA-5.7, respectively. More than that, the treatment of Fe-EDTA combined with pH 5.70 (EDTA-5.7) enhanced nutrient absorption, as proven by the highest tissue contents of P, K, Ca, Mg, Fe, and Mn. The genes' ferric reduction oxidase 1 and 8 (PhFRO1 and PhFRO8), iron-regulated transporter 1 (PhIRT1), nitrate transporter 2.5 (PhNRT2.5), and deoxyhypusine synthase (PhDHS) were expressed at the highest levels in this treatment as well. In the treatment of EDTA-5.7, the reduction and transport of chelated iron in P. hybrida leaves were enhanced, which also affected the transport of nitrate and catalyzed chlorophyll level in leaves. In conclusion, when the medium pH was adjusted to 5.70, supplementation of chelated Fe-EDTA was more conducive to promoting the growth and development of, and absorption of mineral nutrients by, the plant and the expression of related genes in the leaves.

Integrated analysis of single-cell embryo data yields a unified transcriptome signature for the human pre-implantation epiblast.

Single-cell profiling techniques create opportunities to delineate cell fate progression in mammalian development. Recent studies have provided transcriptome data from human pre-implantation embryos, in total comprising nearly 2000 individual cells. Interpretation of these data is confounded by biological factors, such as variable embryo staging and cell-type ambiguity, as well as technical challenges in the collective analysis of datasets produced with different sample preparation and sequencing protocols. Here, we address these issues to assemble a complete gene expression time course spanning human pre-implantation embryogenesis. We identify key transcriptional features over developmental time and elucidate lineage-specific regulatory networks. We resolve post-hoc cell-type assignment in the blastocyst, and define robust transcriptional prototypes that capture epiblast and primitive endoderm lineages. Examination of human pluripotent stem cell transcriptomes in this framework identifies culture conditions that sustain a naïve state pertaining to the inner cell mass. Our approach thus clarifies understanding both of lineage segregation in the early human embryo and of in vitro stem cell identity, and provides an analytical resource for comparative molecular embryology.

Gestational Age-Specific Reference Ranges for the sFlt-1/PlGF Immunoassay Ratio in Twin Pregnancies.

OBJECTIVE: Establish reference ranges for the Elecsys® soluble fms-like tyrosine kinase-1 (sFlt-1)/placental growth factor (PlGF) immunoassay ratio in twin pregnancies. METHODS: Data analyzed were from 3 prospective studies: Prediction of Short-Term Outcome in Pregnant Women with Suspected Preeclampsia (PE) (PROGNOSIS), Study of Early-onset PE in Spain (STEPS), and a multicenter case-control study. Median, 5th, and 95th percentiles for sFlt-1, PlGF, and the sFlt-1/PlGF ratios were determined for normal twin pregnancies for 7 gestational windows and compared with the previous data for singleton pregnancies. RESULTS: The reference range analysis included 269 women with normal twin pregnancies. Before 29 weeks' gestation, median, 5th, and 95th percentiles for sFlt-1/PlGF ratios did not differ between twin and singleton pregnancies. From 29 weeks' gestation to delivery, median, 5th, and 95th percentiles for sFlt-1/PlGF ratios were substantially higher in twin versus singleton pregnancies. sFlt-1 values were higher in women with twin pregnancies across all gestational windows. PlGF values were similar or higher in twin versus singleton pregnancies; PlGF concentrations increased from 10 weeks + 0 days to 28 weeks + 6 days' gestation. CONCLUSIONS: Reference ranges for the sFlt-1/PlGF ratio are similar in women with twin and singleton pregnancies until 29 weeks' gestation but appear higher in twin pregnancies thereafter.

Epigenetic resetting of human pluripotency.

Much attention has focussed on the conversion of human pluripotent stem cells (PSCs) to a more naïve developmental status. Here we provide a method for resetting via transient histone deacetylase inhibition. The protocol is effective across multiple PSC lines and can proceed without karyotype change. Reset cells can be expanded without feeders with a doubling time of around 24 h. WNT inhibition stabilises the resetting process. The transcriptome of reset cells diverges markedly from that of primed PSCs and shares features with human inner cell mass (ICM). Reset cells activate expression of primate-specific transposable elements. DNA methylation is globally reduced to a level equivalent to that in the ICM and is non-random, with gain of methylation at specific loci. Methylation imprints are mostly lost, however. Reset cells can be re-primed to undergo tri-lineage differentiation and germline specification. In female reset cells, appearance of biallelic X-linked gene transcription indicates reactivation of the silenced X chromosome. On reconversion to primed status, XIST-induced silencing restores monoallelic gene expression. The facile and robust conversion routine with accompanying data resources will enable widespread utilisation, interrogation, and refinement of candidate naïve cells.

Effect of Iron Source and Medium pH on Growth and Development of Sorbus commixta In Vitro.

Sorbus commixta is a valuable hardwood plant with a high economical value for its medicinal and ornamental qualities. The aim of this work was to investigate the effects of the iron (Fe) source and medium pH on the growth and development of S. commixta in vitro. The Fe sources used, including non-chelated iron sulfate (FeSO4), iron ethylenediaminetetraacetic acid (Fe-EDTA), and iron diethylenetriaminepentaacetic acid (Fe-DTPA), were supplemented to the Multipurpose medium with a final Fe concentration of 2.78 mg·L-1. The medium without any supplementary Fe was used as the control. The pH of the agar-solidified medium was adjusted to either 4.70, 5.70, or 6.70. The experiment was conducted in a culture room for six weeks with 25 °C day and night temperatures, and a 16-h photoperiod with a light intensity of 50 mmol·m-2·s-1 photosynthetic photon flux density (PPFD). Both the Fe source and pH affected the growth and development of the micropropagated plants in vitro. The leaves were greener in the pH 4.70 and 5.70 treatments. The tissue Fe content decreased with the increase of the medium pH. The leaf chlorophyll content was similar between plants treated with FeSO4 and those with Fe-EDTA. The numbers of the shoots and roots of plantlets treated with FeSO4 were 2.5 and 2 times greater than those of the control, respectively. The fresh and dry weights of the shoot and the root were the greatest for plants treated with Fe-EDTA combined with pH 5.70. The calcium, magnesium, and manganese contents in the plantlets increased in the pH 5.70 treatments regardless of the Fe source. Supplementary Fe decreased the activity of ferric chelate reductase. Overall, although the plantlets absorbed more Fe at pH 4.70, Fe-EDTA combined with pH 5.70 was found to be the best for the growth and development of S. commixta in vitro.

Increased circulating microparticles in streptozotocin-induced diabetes propagate inflammation contributing to microvascular dysfunction.

KEY POINTS: Circulating microparticles (MPs) are elevated in many cardiovascular diseases and have been considered as biomarkers of disease prognosis; however, current knowledge of MP functions has been mainly derived from in vitro studies and their precise impact on vascular inflammation and disease progression remains obscure. Using a diabetic rat model, we identified a >130-fold increase in MPs in plasma of diabetic rats compared to normal rats, the majority of which circulated as aggregates, expressing multiple cell markers and largely externalized phosphatidylserine; vascular images illustrate MP biogenesis and their manifestations in microvessels of diabetic rats. Using combined single microvessel perfusion and systemic cross-transfusion approaches, we delineated how diabetic MPs propagate inflammation in the vasculature and transform normal microvessels into an inflammatory phenotype observed in the microvessels of diabetic rats. Our observations derived from animal studies resembling conditions in diabetic patients, providing a mechanistic insight into MP-mediated pathogenesis of diabetes-associated multi-organ microvascular dysfunction. ABSTRACT: In various cardiovascular diseases, microparticles (MPs), the membrane-derived vesicles released during cell activation, are markedly increased in the circulation. These MPs have been recognized to play diverse roles in the regulation of cellular functions. However, current knowledge of MP function has been largely derived from in vitro studies. The precise impact of disease-induced MPs on vascular inflammation and disease progression remains obscure. In this study we investigated the biogenesis, profile and functional roles of circulating MPs using a streptozotocin-induced diabetic rat model with well-characterized microvascular functions. Our study revealed a >130-fold increase in MPs in the plasma of diabetic rats compared to normal rats. The majority of these MPs originate from platelets, leukocytes and endothelial cells (ECs), and circulate as aggregates. Diabetic MPs show greater externalized phosphatidylserine (PS) than normal MPs. When diabetic plasma or isolated diabetic MPs were perfused into normal microvessels or systemically transfused into normal rats, MPs immediately adhered to endothelium and subsequently mediated leukocyte adhesion. These microvessels then exhibited augmented permeability responses to inflammatory mediators, replicating the microvascular manifestations observed in diabetic rats. These effects were abrogated when MPs were removed from diabetic plasma or when diabetic MPs were pre-coated with a lipid-binding protein, annexin V, suggesting externalized PS to be key in mediating MP interactions with endothelium and leukocytes. Our study demonstrated that the elevated MPs in diabetic plasma are actively involved in the propagation of vascular inflammation through their adhesive surfaces, providing mechanistic insight into the pathogenesis of multi-organ vascular dysfunction that commonly occurs in diabetic patients.

[Ph3 C][B(C6 F5 )4 ]: A Highly Efficient Metal-Free Single-Component Initiator for the Helical-Sense-Selective Cationic Copolymerization of Chiral Aryl Isocyanides and Achiral Aryl Isocyanides.

Commercially available [Ph3 C][B(C6 F5 )4 ] served as a highly efficient metal-free and single-component initiator not only for the carbocationic polymerization of polar and bulky aryl isocyanides with extremely high activity up to 1.2×107  g of polymer/(molcat. h), but also for the helical-sense-selective polymerization of chiral aryl isocyanides and copolymerization with achiral aryl isocyanides to afford high-molecular-weight functional poly(aryl isocyanide)s with good solubility as well as AIE characteristics and/or a single-handed helical conformation.

Functional effector memory T cells contribute to protection from superinfection with heterologous simian immunodeficiency virus or simian-human immunodeficiency virus isolates in Chinese rhesus macaques.

Many studies have revealed a protective effect of infection of an individual with an immunodeficiency virus against subsequent infection with a heterologous strain. However, the extent of protection against superinfection conferred by the first infection and the biological consequences of superinfection are not well understood. Here, we report that a rhesus monkey model of mucosal superinfection was established to investigate the protective immune response. Protection against superinfection was shown to correlate with the extent of the polyfunctionality of CD4+ effector memory T cells, whereas neutralizing antibody responses did not protect against superinfection in this model. Notably, immunodeficiency-virus-associated effector memory T-cell responses might significantly contribute to the suppression of virus superinfection. This provides a potential theoretical basis for the development of an HIV/AIDS vaccine.

Rapid Texture Optimization of Three-Dimensional Urban Model Based on Oblique Images.

Seamless texture mapping is one of the key technologies for photorealistic 3D texture reconstruction. In this paper, a method of rapid texture optimization of 3D urban reconstruction based on oblique images is proposed aiming at the existence of texture fragments, seams, and inconsistency of color in urban 3D texture mapping based on low-altitude oblique images. First, we explore implementing radiation correction on the experimental images with a radiation procession algorithm. Then, an efficient occlusion detection algorithm based on OpenGL is proposed according to the mapping relation between the terrain triangular mesh surface and the images to implement the occlusion detection of the visible texture on the triangular facets as well as create a list of visible images. Finally, a texture clustering algorithm is put forward based on Markov Random Field utilizing the inherent attributes of the images and solve the energy function minimization by Graph-Cuts. The experimental results display that the method is capable of decreasing the existence of texture fragments, seams, and inconsistency of color in the 3D texture model reconstruction.