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Background Recent numerous epidemiology and clinical association studies reported that ApoE polymorphism may associate with the risk and severity of coronavirus disease 2019 (COVID-19), and yielded inconsistent results. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection relies on its spike protein binding to angiotensin-converting enzyme 2 (ACE2) receptor expressed on host cell membranes. Methods A meta-analysis was conducted to clarify the association between ApoE polymorphism and the risk and severity of COVID-19. Multiple protein interaction assays were utilized to investigate the potential molecular link between ApoE and spike protein and between ApoE and also the SARS-CoV-2 primary receptor ACE2. Immunoblotting and immunofluorescence staining methods were used to access the regulatory effect of different ApoE isoform on ACE2 protein expression. Results ApoE gene polymorphism (ε4 carries genotypes VS non-ε4 carries genotypes) is associated with the increased risk (P = 0.0003, OR = 1.44, 95% CI: 1.18–1.76) and progression (P in vitro and in vivo and subsequently decreases the conversion of Ang II to Ang 1–7. Conclusions ApoE4 increases SARS-CoV-2 infectivity in a manner that may not depend on differential interactions with the spike protein or ACE2. Instead, ApoE4 downregulates ACE2 protein expression and subsequently the dysregulation of renin–angiotensin system (RAS) may provide explanation by which ApoE4 exacerbates COVID-19 disease.

This study investigated the accumulation and release risks of heavy metals As, Cd, Co, Cr, Cu, Ni, Pb, and Zn in representative contaminated river-bed and river-side sediments from a groundwater–ri...

Heterogeneity in physical and chemical properties is a common characteristic in a subsurface environment. This study investigated the effect of physico-chemical heterogeneity on arsenic (As) sorption and reactive transport under water extraction in a layered system with preferential flow paths. A flume experiment was performed to derive the spatio-temporal data of As reactive transport. The results indicated that the heterogeneous system significantly accelerated downward (vertical direction) As migration as a coupled effect of physical and chemical heterogeneity that led to fast As transport with low As sorption along the preferential flow paths. The results also indicated that such a heterogeneity effect was driven by water extraction that enhanced the downward groundwater flow along the preferential flow paths. Numerical simulations were performed by matching the experimental results to provide insights into the dominant processes controlling the As migration in the heterogeneous systems. The simulation results highlighted the importance of the kinetic oxidation of mineral-bonded Fe(II) to Fe(III) in the clay matrix that dynamically increased As sorption affinity and retarded As reactive transport. A coupled model of reactive transport along the preferential flow paths, sorption-retarded diffusion from the preferential flow paths into the clay matrixes, and reactions that change sorption affinity in the matrix was required to describe the As reactive transport systems with physico-chemical heterogeneities. The results have strong implications for understanding and modeling As downward migration from shallow to deep aquifers under groundwater pumping conditions in field systems with inherent heterogeneity.

Aims and objectives This research was conducted to explore the effectiveness of employing the healthcare failure mode and effect analysis method in the management of trial of labour after caesarean, with the aims of increasing vaginal birth after caesarean section rate and reducing potential risks that might cause severe complications. Background Previously high caesarean section rate in China and the "two children" policy leads to the situation where multiparas are faced with the choice of another caesarean or trial of labour after caesarean. Despite evidences showing the benefits of vaginal birth after caesarean, obstetricians and midwives in China tend to be conservative due to limited experience and insufficient clinical routines. Thus, its management needs further optimisation in order to make the practice safe and sound. Design A prospective quality improvement programme using the healthcare failure mode and effect analysis. Methods With the structured methodology of healthcare failure mode and effect analysis, we determined core processes of antepartum and intrapartum management, conducted risk priority numbers and devised remedial protocols for failure modes with high risks. The programme was then implemented as a clinical routine under the agreement of the institutional review board and vaginal birth after caesarean success rates were compared before and after the quality improvement programme, both descriptively and statistically. Standards for Quality Improvement Reporting Excellence 2.0 checklist was chosen on reporting the study process. Results Seventy failure modes in seven core processes were identified in the management process, with 14 redressed for actions. The 1-year follow-up trial of labour after caesarean and vaginal birth after caesarean rate was increased compared with the previous 3 years, with a vaginal birth after caesarean rate of 86.36%, whereas the incidence of uterine rupture was not compromised. Conclusions The application of healthcare failure mode and effect analysis can not only promote trial of labour after caesarean and vaginal birth after caesarean rate, but also maintaining a low risk of uterine rupture. Relevance to clinical practice This modified vaginal birth after caesarean management protocol has been shown effective in increasing its successful rate, which can be continued for further comparison of severe complications to the previous practice.

Apple (Malus domestica Borkh.) is an economic backbone driving poverty alleviation and rural revitalization in remote rural areas of China. Monitoring of pathogens associated with apple is particularly important for the apple industry. In 2019, survey for preharvest fruit diseases of apple was conducted in Yanyuan County, which lies on the southern edge of the Qinghai-Tibet Plateau, Sichuan, China. In one commercial orchard (27°26'49.8"N, 101°39'38.9"E), an uncharacterized fruit rot disease was observed on 'Red Fuji Nagafu No. 2' apple with prevalence of approximately 3%. Symptoms on the fruits occurred as light brown spots about 3 millimeters in diameter. With the progression of the disease, the originally infected sites turned deep brown, lesions expanded and decayed tissues became spongy. Ultimately, multiple lesions coalesced together, severely infected fruits became sunken, soft, wrinkled, and decayed completely. Twenty samples with typical symptoms were collected. Symptomatic apple tissues from the lesion margin were cut into 5 × 5 mm pieces, washed two times with 70% ethanol, disinfected with 0.5% NaClO for 5 min, rinsed twice with sterile double-distilled water, and plated on potato dextrose agar (PDA) medium at 20 °C in darkness for 5 days. Forty-five colonies were isolated from symptomatic tissues on PDA after 3 days and they shared similar morphology. Five single-spore isolates were obtained and a representative isolate designated ABT12-1 was characterized further (CCTCC accession no. M2021680) (Chaverri et al. 2011). The fungal colonies produced radial, abundant cottony aerial mycelium, white-saffron to saffron-ochraceous in color, and the reverse colony was ochraceous to sienna with yellow pigmentation in the agar. Conidiophores were observed developing laterally from aerial hyphae, irregularly branched or in fascicles, 1-4 branched, 21.5 to 87.1 μm long by 3.5 to 7.8 μm wide (n=20). Phialides were generally long and cylindrical or somewhat flask-shaped. Microconidia were generally ellipsoidal, with 0-1 septations and measured 3.2 to 16.6 × 2.5 to 7.2 μm (n=20). Macroconidia were ellipsoidal, oblong to long cylindrical, hyaline, smooth, slightly curved and round at both ends, with 3-7 septations, and averaged 45 × 4 μm (n=20). The fungus was initially identified as a member of the genus Neonectria based on the morphological observations (Lombard et al. 2015). Molecular identification was performed to determine fungal species by sequencing partial actin (Act), internal transcribed spacer (ITS), large subunit of ribosomal DNA (LSU), RNA polymerase II subunit one (Rpb1), translation elongation factor 1-α (Tef1), and the beta-tubulin (Tub) genes, which were amplified with primers Tact1/Tact2, ITS5/ITS4, LR5/LROR, crpb1a/rpb1c, tef1-728/tef1-986 and Btub-T1/Btub-T2, respectively (Carbone and Kohn 1999; Castlebury et al. 2006; O'Donnell and Cigelnik 1997; Schoch et al. 2012; White et al. 1990). The resulting sequences were deposited in GenBank (accession no. MW538899 for Act; MW534396 for ITS; MW534401 for LSU; MW538900 for Rpb1; MW538901 for Tef1; and MW538902 for Tub). Multilocus phylogenetic analysis with neighbor-joining methods based on the above 6 gene sequences showed that the fungal isolate clustered with Neonectria punicea (J.C. Schmidt) Castl. & Rossman. To test the pathogenicity, ten freshly picked 'Red Fuji' apple fruits were wound-inoculated with 2 µl of conidial suspension (1 × 105 conidia/ml) of the isolate ABT12-1; sterile water was used as control. The inoculated samples were placed in sterilized plastic boxes to maintain relative humidity and incubated at 20 °C for seven days. Pathogenicity experiments were conducted four times. After three days, the wound sites inoculated with conidial suspension showed visible diseased spots. As lesions progressively dilated, symptoms similar to those of the decayed fruit in the field were observed, whereas the control fruits remained symptomless. The pathogen was reisolated from symptomatic lesions, thus fulfilling Koch's postulates. Neonectria punicea causes stem and bark canker diseases on a variety of trees (Hirooka et al. 2013; Karadžic et al. 2020; Salgado-Salazar and Crouch 2019). To our knowledge, N. punicea has never been reported causing apple fruit rot in China.

Macroautophagy/autophagy and necroptosis represent two opposing cellular s tress responses. Whereas autophagy primarily fulfills a cyto-protective function, necroptosis is a form of regulated cell death induced via death receptors. Here, we aimed at investigating the molecular crosstalk between these two pathways. We observed that RIPK3 directly associates with AMPK and phosphorylates its catalytic subunit PRKAA1/2 at T183/T172. Activated AMPK then phosphorylates the autophagy-regulating proteins ULK1 and BECN1. However, the lysosomal degradation of autophagosomes is blocked by TNF-induced necroptosis. Specifically, we observed dysregulated SNARE complexes upon TNF treatment; e.g., reduced levels of full-length STX17. In summary, we identified RIPK3 as an AMPK-activating kinase and thus a direct link between autophagy- and necroptosis-regulating kinases. Abbreviations: ACACA/ACC: acetyl-CoA carboxylase alpha; AMPK: AMP-activated protein kinase; ATG: autophagy-related; BECN1: beclin 1; GFP: green fluorescent protein; EBSS: Earle’s balanced salt solution; Hs: Homo sapiens; KO: knockout; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MEF: mouse embryonic fibroblast; MLKL: mixed lineage kinase domain like pseudokinase; Mm: Mus musculus; MTOR: mechanistic target of rapamycin kinase; MVB: multivesicular body; PIK3C3/VPS34: phosphatidylinositol 3-kinase catalytic subunit type 3; PIK3R4/VPS15: phosphoinositide-3-kinase regulatory subunit 4; PLA: proximity ligation assay; PRKAA1: protein kinase AMP-activated catalytic subunit alpha 1; PRKAA2: protein kinase AMP-activated catalytic subunit alpha 2; PRKAB2: protein kinase AMP-activated non-catalytic subunit beta 2; PRKAG1: protein kinase AMP-activated non-catalytic subunit gamma 1; PtdIns3K: phosphatidylinositol 3-kinase; PtdIns3P: phosphatidylinositol-3-phosphate; RIPK1: receptor interacting serine/threonine kinase 1; RIPK3: receptor interacting serine/threonine kinase 3; SNAP29: synaptosome associated protein 29; SNARE: soluble N-ethylmaleimide-sensitive factor attachment protein receptor; SQSTM1/p62: sequestosome 1; STK11/LKB1: serine/threonine kinase 11; STX7: syntaxin 7; STX17: syntaxin 17; TAX1BP1: Tax1 binding protein 1; TNF: tumor necrosis factor; ULK1: unc-51 like autophagy activating kinase 1; VAMP8: vesicle associated membrane protein 8; WT: wild-type.

The mammalian ULK1 is the central initiating kinase of bulk and selective macroautophagy/autophagy processes. In the past, both autophagy-relevant and non-autophagy-relevant substrates of this Ser/Thr kinase have been reported. Here, we describe our recent finding that ULK1 also regulates TNF signaling pathways. We find that inhibition of autophagy or specifically ULK1 increases TNF-induced cell death. This autophagy-independent pro-survival function of ULK1 is mediated via the phosphorylation of RIPK1 at Ser357. RIPK1 is the central mediator of pro-inflammatory or pro-death signaling pathways induced by TNF, and ULK1-dependent phosphorylation regulates RIPK1 activation and distribution to different intracellular signaling complexes. Our results indicate that ULK1 exerts a cyto-protective function not only by initiating autophagy, but also by controlling RIPK1-mediated cell death.

Summary: The evolutionarily conserved ULK1 kinase complex acts as gatekeeper of canonical autophagy and regulates induction of autophagosome biogenesis. To better understand control of ULK1 and analyze whether ULK1 has broader functions that are also linked to the later steps of autophagy, we perform comprehensive phosphoproteomic analyses. Combining in vivo with in vitro data, we identify numerous direct ULK1 target sites within autophagy-relevant proteins that are critical for autophagosome maturation and turnover. In addition, we highlight an intimate crosstalk between ULK1 and several phosphatase complexes. ULK1 is not only a PP2A target but also directly phosphorylates the regulatory PP2A subunit striatin, activating PP2A and serving as positive feedback to promote autophagy-dependent protein turnover. Thus, ULK1 and phosphatase activities are tightly coordinated to robustly regulate protein degradation by autophagy.

Cisplatin-based treatment is the standard of care therapy for urothelial carcinomas. However, complex cisplatin resistance mechanisms limit the success of this approach. Both apoptosis and autophagy have been shown to contribute to this resistance. Prodigiosin, a secondary metabolite from various bacteria, exerts different biological activities including the modulation of these two cellular stress response pathways. We analyzed the effect of prodigiosin on protein levels of different autophagy- and apoptosis-related proteins in cisplatin-sensitive and -resistant urothelial carcinoma cells (UCCs). Furthermore, we investigated the effect on cell viability of prodigiosin alone or in combination with cisplatin. We made use of four different pairs of cisplatin-sensitive and -resistant UCCs. We found that prodigiosin blocked autophagy in UCCs and re-sensitized cisplatin-resistant cells to apoptotic cell death. Furthermore, we found that prodigiosin is a potent anticancer agent with nanomolar IC50 values in all tested UCCs. In combination studies, we observed that prodigiosin sensitized both cisplatin-sensitive and -resistant urothelial carcinoma cell lines to cisplatin treatment with synergistic effects in most tested cell lines. These effects of prodigiosin are at least partially mediated by altering lysosomal function, since we detected reduced activities of cathepsin B and L. We propose that prodigiosin is a promising candidate for the therapy of cisplatin-resistant urothelial carcinomas, either as a single agent or in combinatory therapeutic approaches.

Receptor interacting serine/threonine kinase 1 (RIPK1) is the central mediator of tumor necrosis factor (TNF) signaling. It regulates both pro-survival/pro-inflammatory and cell death pathways. In order to fulfill this complex regulation, RIPK1 is regulated by several post-translational modifications, including ubiquitination, acetylation, and phosphorylation. In our recent work, we show that the unc-51-like autophagy activating kinase 1 (ULK1) phosphorylates RIPK1 at Ser357 and thus blocks TNF-induced cell death.

Mitochondria are cellular organelles with crucial functions in the generation and distribution of ATP, the buffering of cytosolic Ca2+ and the initiation of apoptosis. Compounds that interfere with these functions are termed mitochondrial toxins, many of which are derived from microbes, such as antimycin A, oligomycin A, and ionomycin. Here, we identify the mycotoxin phomoxanthone A (PXA), derived from the endophytic fungus Phomopsis longicolla, as a mitochondrial toxin. We show that PXA elicits a strong release of Ca2+ from the mitochondria but not from the ER. In addition, PXA depolarises the mitochondria similarly to protonophoric uncouplers such as CCCP, yet unlike these, it does not increase but rather inhibits cellular respiration and electron transport chain activity. The respiration-dependent mitochondrial network structure rapidly collapses into fragments upon PXA treatment. Surprisingly, this fragmentation is independent from the canonical mitochondrial fission and fusion mediators DRP1 and OPA1, and exclusively affects the inner mitochondrial membrane, leading to cristae disruption, release of pro-apoptotic proteins, and apoptosis. Taken together, our results suggest that PXA is a mitochondrial toxin with a novel mode of action that might prove a useful tool for the study of mitochondrial ion homoeostasis and membrane dynamics.

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Micro-grids(MGs) with distributed generation (DG) provide a resilient solution in the case of major faults in a distribution system due to natural disasters. A resilience-oriented load restoration models that the energy will be supplied by DGs to hold maximum loads satisfying operation constraints is proposed in this paper. The virtual node and virtual branch are introduced to guarantee the topology of distribution systems. The outputs of the patchable and dis-patchable DGs and the sustainable power supply capacity will be considered. For the nonlinear characteristics of the proposed mathematical model, the piecewise linearization method is used to linearize the power flow constraints. Hence, the load restoration model for the distribution system is transformed into a mixed integer linear programming (MILP) problem. Numerical results based on modified IEEE-33 distribution test systems validate the effectiveness of our proposed method.

Summary: Autophagy, apoptosis, and necroptosis are stress responses governing the ultimate fate of a cell. However, the crosstalk between these cellular stress responses is not entirely understood. Especially, it is not clear whether the autophagy-initiating kinase ULK1 and the cell-death-regulating kinase RIPK1 are involved in this potential crosstalk. Here, we identify RIPK1 as a substrate of ULK1. ULK1-dependent phosphorylation of RIPK1 reduces complex IIb/necrosome assembly and tumor necrosis factor (TNF)-induced cell death, whereas deprivation of ULK1 enhances TNF-induced cell death. We observe that ULK1 phosphorylates multiple sites of RIPK1, but it appears that especially phosphorylation of S357 within the intermediate domain of RIPK1 mediates this cell-death-inhibiting effect. We propose that ULK1 is a regulator of RIPK1-mediated cell death. : Wu et al. show that the autophagy-inducing kinase ULK1 phosphorylates the necroptosis-regulating kinase RIPK1 within its intermediate domain at Ser357. This phosphorylation reduces the assembly of the death-inducing complex IIb/necrosome and, thus, TNF-induced cell death. Keywords: ULK1, RIPK1, RIPK3, autophagy, necroptosis, TNF, MLKL, necrosome, complex I, complex II

In the context of smart grids, generation expansion planning is confronted with many uncertain factors, such as renewable energy penetration, users’ options, applications of new technologies, etc. However, some of the uncertainties may only have partial information, making it difficult to use a traditional optimization method to solve the planning problems. In this paper, a robust two-stage stochastic programming model is investigated to handle generation expansion planning problems with incomplete information of uncertainties. In this model, it is assumed that the availability of the first and second moments information of random variables is known. By adopting the duality technique and an affine rule, the proposed two-stage stochastic programming problem can be reformulated as a deterministic second-order cone optimization problem under the robust optimization paradigm. A tractable mathematical model is derived, which minimizes the investment and operational costs subjected to system constraints. Case studies illustrate that an expansion solution always can be obtained under uncertainties with incomplete information. Sensitivity analysis is also conducted, which demonstrates that the robustness of optimal expansion decision depends on the levels of uncertainties.

Macroautophagy/autophagy is an evolutionarily conserved cellular process whose induction is regulated by the ULK1 protein kinase complex. The subunit ATG13 functions as an adaptor protein by recruiting ULK1, RB1CC1 and ATG101 to a core ULK1 complex. Furthermore, ATG13 directly binds both phospholipids and members of the Atg8 family. The central involvement of ATG13 in complex formation makes it an attractive target for autophagy regulation. Here, we analyzed known interactions of ATG13 with proteins and lipids for their potential modulation of ULK1 complex formation and autophagy induction. Targeting the ATG101-ATG13 interaction showed the strongest autophagy-inhibitory effect, whereas the inhibition of binding to ULK1 or RB1CC1 had only minor effects, emphasizing that mutations interfering with ULK1 complex assembly do not necessarily result in a blockade of autophagy. Furthermore, inhibition of ATG13 binding to phospholipids or Atg8 proteins had only mild effects on autophagy. Generally, the observed phenotypes were more severe when autophagy was induced by MTORC1/2 inhibition compared to amino acid starvation. Collectively, these data establish the interaction between ATG13 and ATG101 as a promising target in disease-settings where the inhibition of autophagy is desired.

UNC-51 like kinase (ULK1) translocates to dysfunctional mitochondria and is involved in mitophagy, but the mechanisms responsible for ULK1 activation and translocation remain unclear. Here, we found that hypoxia induces phosphorylation of ULK1 at Serine-555 by Adenosine 5′-monophosphate (AMP)-activated protein kinase (AMPK). Unlike wild-type ULK1, an ULK1 (S555A) mutant cannot translocate to mitochondria in response to hypoxia. Inhibition or knockdown of AMPK prevents ULK1 translocation and inhibits mitophagy. Finally, the phospho-mimic ULK1 (S555D) mutant, but not ULK1 (S555A), rescues mitophagy in AMPK-knockdown cells. Thus, we conclude that AMPK-dependent phosphorylation of ULK1 is critical for translocation of ULK1 to mitochondria and for mitophagy in response to hypoxic stress.

Mitophagy receptors mediate the selective recognition and targeting of damaged mitochondria by autophagosomes. The mechanism for the regulation of these receptors remains unknown. Here, we demonstrated that a novel hypoxia-responsive microRNA, microRNA-137 (miR-137), markedly inhibits mitochondrial degradation by autophagy without affecting global autophagy. miR-137 targets the expression of two mitophagy receptors NIX and FUNDC1. Impaired mitophagy in response to hypoxia caused by miR-137 is reversed by re-expression of FUNDC1 and NIX expression vectors lacking the miR-137 recognition sites at their 3' UTR. Conversely, miR-137 also suppresses the mitophagy induced by fundc1 (CDS+3'UTR) but not fundc1 (CDS) overexpression. Finally, we found that miR-137 inhibits mitophagy by reducing the expression of the mitophagy receptor thereby leads to inadequate interaction between mitophagy receptor and LC3. Our results demonstrated the regulatory role of miRNA to mitophagy receptors and revealed a novel link between miR-137 and mitophagy.

Autophagy eliminates dysfunctional mitochondria in an intricate process known as mitophagy. ULK1 is critical for the induction of autophagy, but its substrate(s) and mechanism of action in mitophagy remain unclear. Here, we show that ULK1 is upregulated and translocates to fragmented mitochondria upon mitophagy induction by either hypoxia or mitochondrial uncouplers. At mitochondria, ULK1 interacts with FUNDC1, phosphorylating it at serine 17, which enhances FUNDC1 binding to LC3. A ULK1-binding-deficient mutant of FUNDC1 prevents ULK1 translocation to mitochondria and inhibits mitophagy. Finally, kinase-active ULK1 and a phospho-mimicking mutant of FUNDC1 rescue mitophagy in ULK1-null cells. Thus, we conclude that FUNDC1 regulates ULK1 recruitment to damaged mitochondria, where FUNDC1 phosphorylation by ULK1 is crucial for mitophagy.

Cyanobacterial blooms in freshwaters have become one of the most widespread of environmental problems and threaten water resources worldwide. Previous studies on cyanobacteria in Lake Taihu often collected samples from one site (like Meiliang Bay or Zhushan Bay) and focused on the variation in patterns or abundance of Microcystis during the blooming season. However, the distribution of cyanobacteria in Lake Taihu shows differing pattern in various seasons. In this study, water samples were collected monthly for one year at five sites in Lake Taihu with different trophic status and a physicochemical analysis and denaturing gradient gel electrophoresis (DGGE) were conducted. DGGE fingerprint analysis showed that Microcystis (7/35 bands) and Synechococcus (12/35 bands) were the two most dominant genera present during the study period at all five sites. Cyanobium (3/35 bands) was the third most common genus which has seldom been previously reported in Lake Taihu. Redundancy analysis (RDA) indicated that the cyanobacterial community structure was significantly correlated with NO3 --N, CODMn, and NH4 +-N in the winter and spring, whereas it was correlated with water temperature in the summer and autumn. Limiting the nutrient input (especially of N and C loading) in Lake Taihu would be a key factor in controlling the growth of different genera of cyanobacteria.

In hypoxic cells, dysfunctional mitochondria are selectively removed by a specialized autophagic process called mitophagy. The ER-mitochondrial contact site (MAM) is essential for fission of mitochondria prior to engulfment, and the outer mitochondrial membrane protein FUNDC1 interacts with LC3 to recruit autophagosomes, but the mechanisms integrating these processes are poorly understood. Here, we describe a new pathway mediating mitochondrial fission and subsequent mitophagy under hypoxic conditions. FUNDC1 accumulates at the MAM by associating with the ER membrane protein calnexin. As mitophagy proceeds, FUNDC1/calnexin association attenuates and the exposed cytosolic loop of FUNDC1 interacts with DRP1 instead. DRP1 is thereby recruited to the MAM, and mitochondrial fission then occurs. Knockdown of FUNDC1, DRP1, or calnexin prevents fission and mitophagy under hypoxic conditions. Thus, FUNDC1 integrates mitochondrial fission and mitophagy at the interface of the MAM by working in concert with DRP1 and calnexin under hypoxic conditions in mammalian cells.

Poly(allylamine-co- N,N’ -methylenebisacrylamide) magnetic nanogels (PAAm-Fe3O4) were prepared by photochemical polymerization of allylamine and N,N′ -methylenebisacrylamide in magnetite aqueous suspension under UV irradiation. The composition, zeta potential, morphology, particle size distribution and magnetic properties of the product were characterized in detail. To explore the initiating process of polymerization, laser flash photolysis was used to investigate the interaction between Fe3O4 nanoparticles and organic electron donor by employing aniline as the probe molecule, an analogue of allylamine. It indicated an occurrence of electron transfer process from the organic electron donor to Fe3O4 which may be critical to initiate polymerization reaction of amino monomer and form polymer shell on the surface of Fe3O4 nanoparticles. The mean diameter and diameter distribution of PAAm-Fe3O4 can be tuned in a moderate range by varing irradiation time or volume of the dropped monomer. The experimental results also proved that nearly spherical PAAm-Fe3O4 possessed a core-shell structure and positive zeta potential and high magnetic content of nearly 88%. Moreover, it behaved quasi-superparamagnetic at room temperature and its saturation magnetization reached to 50 emu/g. Finally, a possible formation mechanism of magnetic nanogel was proposed.