Adult Neurogenesis and the Initiation of Social Aggression in Male Mice.

The hippocampus is important for social behavior and exhibits unusual structural plasticity in the form of continued production of new granule neurons throughout adulthood, but it is unclear how adult neurogenesis contributes to social interactions. In the present study, we suppressed neurogenesis using a pharmacogenetic mouse model and examined social investigation and aggression in adult male mice to investigate the role of hippocampal adult-born neurons in the expression of aggressive behavior. In simultaneous choice tests with stimulus mice placed in corrals, mice with complete suppression of adult neurogenesis in adulthood (TK mice) exhibited normal social investigation behaviors, indicating that new neurons are not required for social interest, social memory, or detection of and response to social olfactory signals. However, mice with suppressed neurogenesis displayed decreased offensive and defensive aggression in a resident-intruder paradigm, and less resistance in a social dominance test, relative to neurogenesis-intact controls, when paired with weight and strain-matched (CD-1) mice. During aggression tests, TK mice were frequently attacked by the CD-1 intruder mice, which never occurred with WTs, and normal CD-1 male mice investigated TK mice less than controls when corralled in the social investigation test. Importantly, TK mice showed normal aggression toward prey (crickets) and smaller, nonaggressive (olfactory bulbectomized) C57BL/6J intruders, suggesting that mice lacking adult neurogenesis do not avoid aggressive social interactions if they are much larger than their opponent and will clearly win. Taken together, our findings show that adult hippocampal neurogenesis plays an important role in the instigation of intermale aggression, possibly by weighting a cost-benefit analysis against confrontation in cases where the outcome of the fight is not clear.

A pilot study examining periodontally healthy middle-aged humans and monkeys display different levels of alveolar bone resorption, gingival inflammatory infiltrate, and salivary microbiota profile.

BACKGROUND: Monkeys are an appropriate model for periodontal research owing to their similar dental anatomy and physiology unlike humans. Extensive literature exists on pathological periodontitis in monkeys and humans, although concerns regarding whether healthy middle-aged monkeys and humans display the same periodontal and oral microbial status remains unclear. AIMS AND OBJECTIVES: The current study aimed to compare alveolar bone resorption, gingival inflammatory infiltrate, and salivary microbiota profile in periodontally healthy middle-aged humans and monkeys. METHODS: CBCT examination and histological analysis were performed to compare the periodontal status in middle-aged healthy humans and monkeys. Oral saliva16S rRNA sequencing was performed to analyze the oral microbial profile. RESULTS: The alveolar resorption was compared between humans and monkeys, to determine the periodontal health. The percentage attachment of attachment loss was more around the posteriors teeth in humans when compared to monkeys (p<0.05). The degree of gingival inflammation was analyzed in both the groups, the expression of CD 34,45was higher in humans. 16S rRNA analysis demonstrated less diversity of salivary microorganisms in humans than in monkeys. The relative abundance of Aggregatibacter, Haemophilus, Gemella, and Porphyromonas at the genus level was significantly less in humans than in monkeys (p(<0.05). CONCLUSION: The periodontally healthy middle-aged humans and monkeys display different alveolar bone resorption and gingival inflammatory infiltrate levels. Furthermore, the salivary microbiota profile showed distinctly different oral microbiomes in these two primates. Our results suggest that the difference in alveolar bone status and gingival inflammatory infiltrate in healthy humans and monkeys might be associated with the diversity of the oral microbiome.

The therapeutic effect and possible mechanisms of alginate oligosaccharide on metabolic syndrome by regulating gut microbiota.

Metabolic syndrome (MetS) is a disease condition incorporating the abnormal accumulation of various metabolic components, including overweight or abdominal obesity, insulin resistance and abnormal glucose tolerance, hypertension, atherosclerosis, or dyslipidemia. It has been proved that the gut microbiota and microbial-derived products play an important role in regulating lipid metabolism and thus the onset and development of MetS. Previous studies have demonstrated that oligosaccharides with prebiotic effects, such as chitosan oligosaccharides, can regulate the structure of the microbial community and its derived products to control weight and reduce MetS associated with obesity. Alginate oligosaccharides (AOS), natural products extracted from degraded alginate salts with high solubility and extensive biological activity, have also been found to modulate gut microbiota. This review aims to summarize experimental evidence on the positive effects of AOS on different types of MetS while providing insights into mechanisms through which AOS regulates gut microbiota for preventing and treating MetS.

TRIM24-DTNBP1-ATP7A mediated astrocyte cuproptosis in cognition and memory dysfunction caused by Y2O3 NPs.

Yttrium oxide nanoparticles (Y2O3 NPs), extensively utilized rare earth nanoparticles, exhibited a diverse range of applications across various fields, which leading to increased human exposure. Moreover, potential neurotoxic risks have been associated with their use, yet the underlying mechanism remains unclear. The present study aimed to investigate the effects of Y2O3 NPs on cognitive function in rats with a particular focus on elucidating the pivotal role played by astrocytes in this process. The results demonstrated that Y2O3 NPs induced cognitive and memory impairment in rats, copper (Cu) accumulation and cuproptosis of astrocytes as contributing factors. Furthermore, we elucidated that Y2O3 NPs induced astrocytes cuproptosis by inhibiting TRIM24/DTNBP1/ATP7A signaling pathway-mediated cellular Cu efflux. We provide, for the first time, the important involvement of astrocytes in Y2O3 NPs-induced neurotoxicity, elucidating that cuproptosis as the primary mode of cell death. These results offer valuable insights for the future safe application of rare earth nanoparticles in field of neurology.

Starvation-induced phosphorylation activates gasdermin A to initiate pyroptosis.

Pyroptosis, a pro-inflammatory form of programmed cell death, is crucial for host defense against pathogens and danger signals. Proteolytic cleavage of gasdermin proteins B-E (GSDMB-GSDME) is well established as a trigger for pyroptosis, but the intracellular activation mechanism of GSDMA remains elusive. Here, we demonstrate that severe starvation induces pyroptosis through phosphorylation-induced activation of GSDMA. Nutrient stresses stimulate GSDMA activation via phosphorylation mediated by Unc-51-like autophagy-activating kinase 1 (ULK1). Phosphorylation of Ser353 on human GSDMA by ULK1 or the phospho-mimetic Ser353Asp mutant of GSDMA liberates GSDMA from auto-inhibition, facilitating its membrane targeting and initiation of pyroptosis. To further validate the significance of GSDMA phosphorylation, we generated a constitutively active mutant Ser354Asp of mouse Gsdma, which induced skin inflammation and hyperplasia in mice, reminiscent of phenotypes with activated Gsdma. This study uncovers phosphorylation of GSDMA as a mechanism underlying pyroptosis initiation and cellular response to nutrient stress.

Tuning the structure and properties of carbon cloth by FeCl3intercalation for efficient two-electron oxygen reduction catalysis.

The advancement of various energy conversion and storage technologies hinges on the development of efficient and stable electrocatalysts for the oxygen reduction reaction (ORR). In this study, we report the enhancement of carbon cloth (CC) for robust ORR through an FeCl3intercalation reaction. Utilizing a thermal annealing method, FeCl3was intercalated into the graphite structure on the surface of CC, resulting in the creation of numerous defects and the incorporation of Fe species. These newly introduced defects play a pivotal role in activating the ORR via a two-electron pathway. The presence of Fe species further stabilizes the catalytic activity, leading to efficient and stable ORR performance. Our findings highlight the significance of defect engineering and Fe species incorporation in carbon-based materials for improved ORR catalysis and pave the way for the development of advanced electrocatalysts for energy-related applications.

Copper-Catalyzed Oxyfluorosulfonylation of ß,γ-Unsaturated Oximes with Sulfur Dioxide and Selectfluor for Isoxazoline-Functionalized Aliphatic Sulfonyl Fluorides.

In this report, we describe a copper-catalyzed cascade reaction involving oxygen radical-induced cyclization/SO2 insertion/fluorination of ß,γ-unsaturated oximes with sulfur dioxide and Selectfluor under mild conditions for the synthesis of isoxazoline-functionalized aliphatic sulfonyl fluorides. The synthetic potential of these compounds has been evaluated through diverse SuFEx reactions.

Antibacterial activity of a polysaccharide isolated from litchi (Litchi chinensis Sonn.) pericarp against Staphylococcus aureus and the mechanism investigation.

The long-term use of antibiotics can cause drug resistance. Natural polysaccharides are a novel means of treating bacterial infections, and the development and utilization of litchi pericarp polysaccharide (LPPs) as a bacteriostatic active substance offer a new research direction for the high-value utilization of litchi by-products. This study revealed that LPPs inhibited Staphylococcus aureus more than Escherichia coli, Listeria monocytogenes, and Salmonella typhimurium, with the minimum inhibitory concentrations of 145, 205, 325, and 445 µg/mL, respectively. The inhibitory activity of LPPs was insignificant for Bacillus subtilis at 505 µg/mL. The assessment of antibacterial mechanisms revealed that LPPs influenced the growth, conductivity, protein, and nucleic acid, reducing sugar, respiratory chain dehydrogenase activity, bacterial lipid peroxidation, intracellular adenosine triphosphate, and extracellular alkaline phosphatase levels of S. aureus. Of note, LPPs could modify the cell wall integrity and cell membrane permeability of S. aureus, resulting in the leakage of intracellular large and small molecules, inhibition of cellular respiratory metabolism, and oxidative losses. These processes exhibited an inhibitory effect and made the bacterium nonfunctional, thereby affecting its growth and metabolism or causing cell death. These findings provide support and insights into the potential application of LPPs as a natural antimicrobial agent.

Synergistic Crystallization Modulation and Defects Passivation in Kesterite via Anion-Coordinate Precursor Engineering for Efficient Solar Cells.

It has been validated that enhancing crystallinity and passivating the deep-level defect are critical for improving the device performance of kesterite Cu2ZnSn(S,Se)4 (CZTSSe) solar cells. Coordination chemistry interactions within the Cu-Zn-Sn-S precursor solution play a crucial role in the management of structural defects and the crystallization kinetics of CZTSSe thin films. Therefore, regulating the coordination environment of anion and cation in the precursor solution to control the formation process of precursor films is a major challenge at present. Herein, a synergetic crystallization modulation and defect passivation method is developed using P2S5 as an additive in the CZTS precursor solution to optimize the coordination structure and improve the crystallization process. The alignment of theoretical assessments with experimental observations confirms the ability of the P2S5 molecule to coordinate with the metal cation sites of CZTS precursor films, especially more liable to the Zn2+, effectively passivating the Zn-related defects, thereby significantly reducing the defect density in CZTSSe absorbers. As a result, the device with a power conversion efficiency of 14.36% has been achieved. This work provides an unprecedented strategy for fabricating high-quality thin films by anion-coordinate regulation and a novel route for realizing efficient CZTSSe solar cells.

Trajectories of acute gastrointestinal injury grade in critically Ill children.

OBJECTIVE: To investigate the characteristics of different Acute Gastrointestinal Injury (AGI) grading trajectories and examine their impact on prognosis in the Pediatric Intensive Care Unit (PICU). METHODS: This retrospective cohort study was conducted at a large children's hospital in China. The children admitted to the PICU were included. AGI grade was assessed every other day during the initial nine days following PICU admission. RESULTS: A total of 642 children were included, of which 364 children (56.7%) exhibited varying degrees of gastrointestinal dysfunction (AGI grade ≥ 2). Based on the patterns of AGI grading over time, six groups were identified: low-stable group, low-fluctuating group, medium-decreasing group, medium-increasing group, high-decreasing group, high-persistent group. The high-persistent group accounted for approximately 90% of all recorded deaths. Compared to low-stable group, both the medium-increasing and high-persistent groups exhibited positive correlations with length of stay in PICU (PICU LOS) and length of stay (LOS). Compared to low-stable group, the five groups exhibited a negative correlation with the percentage of energy received by enteral nutrition (EN), as well as the protein received by EN. CONCLUSION: This study identified six distinct trajectory groups of AGI grade in critically ill children. The pattern of AGI grade trajectories over time were associated with EN delivery proportions and clinical outcomes.

Carbon Dots Derived from Non-Biomass Waste: Methods, Applications, and Future Perspectives.

Carbon dots (CDs) are luminescent carbon nanoparticles with significant potential in analytical sensing, biomedicine, and energy regeneration due to their remarkable optical, physical, biological, and catalytic properties. In light of the enduring ecological impact of non-biomass waste that persists in the environment, efforts have been made toward converting non-biomass waste, such as ash, waste plastics, textiles, and papers into CDs. This review introduces non-biomass waste carbon sources and classifies them in accordance with the 2022 Australian National Waste Report. The synthesis approaches, including pre-treatment methods, and the properties of the CDs derived from non-biomass waste are comprehensively discussed. Subsequently, we summarize the diverse applications of CDs from non-biomass waste in sensing, information encryption, LEDs, solar cells, and plant growth promotion. In the final section, we delve into the future challenges and perspectives of CDs derived from non-biomass waste, shedding light on the exciting possibilities in this emerging area of research.

Changes in the Biomechanical Properties of Corneal Stromal Lens after Collagen Crosslinking Induced by EDC-NHS.

Introduction: To evaluate the changes of lens antidilatation, antiedema, and antienzymolysis ability after different concentrations of 1-ethyl-3-(3-dimethylaminopropyl) carbodiimide and N-hydroxysuccinimide (EDC-NHS)-induced collagen cross-linking. Methods: Corneal stromal lenticules (n = 100) obtained from small incision lenticule extraction (SMILE) procedures were divided into 5 groups: no treatment (control); EDC/NHS (5%/2.5%); EDC/NHS(5%/5%); EDC/NHS (10%/5%); riboflavin and ultraviolet-A light (UVA). Collagen crosslinking was induced using EDC-NHS and UVA. Biomechanical assessments including inflation test, enzymatic degradation resistance, and light transmittance were evaluated posttreatment. Results: (1) Lenticule apex displacement ranked: control Group > UVA Group > Group (5%/5%) > Group (5%/2.5%) > Group (10%/5%) (Friedman test, p < 0.0001). (2) Light transmittance was significantly higher in the crosslinked groups versus control, with EDC/NHS superior to UVA riboflavin. After 15 minutes in PBS, light transmittance decreased due to swelling; however, crosslinked groups maintained significantly higher transmittance versus control. (3) Following crosslinking, enzymatic resistance improved significantly, with the EDC-NHS crosslinking group was significantly better than the UVA cross-linking group. Conclusions: EDC/NHS crosslinking enhanced lenticule stiffness, antiedema, and enzymatic resistance and without compromising the transparency of the lens. Moreover, EDC/NHS crosslinking efficacy exceeded UVA riboflavin crosslinking in improving lenticule biomechanical properties.

Chemical Doping and O-Functionalization of Carbon-Based Electrode to Improve Vanadium Redox Flow Batteries.

The vanadium redox flow battery (VRFB) holds promise for large-scale energy storage applications, despite its lower energy and power densities compared to advanced secondary batteries available today. Carbon materials are considered suitable catalyst electrodes for improving many aspects of the VRFB. However, pristine graphite structures in carbon materials are catalytically inert and require modification to activate their catalytic activity. Among the various strategies developed so far, O-functionalization and chemical doping of carbon materials are considered some of the most promising pathways to regulate their electronic structures. Building on the catalytic mechanisms involved in the VRFB, this concise review discusses recent advancements in the O-functionalization and chemical doping of carbon materials. Furthermore, it explores how these materials can be tailored and highlights future directions for developing more promising VRFBs to guide future research.

SAP deletion promotes malignant insulinoma progression by inducing CXCL12 secretion from CAFs via the CXCR4/p38/ERK signalling pathway.

Malignant insulinoma is an extremely rare type of functioning pancreatic neuroendocrine tumour with a high degree of malignancy and a high incidence of metastasis. However, it is still unclear how malignant insulinomas develop and metastasize. Serum amyloid P component (SAP), a member of the pentraxin protein family, is an acute-phase protein secreted by liver cells. The role of SAP in insulinoma and the related mechanism are still unknown. To determine the effect of SAP on insulinoma, we crossed Rip1-Tag2 mice, which spontaneously develop insulinoma, and SAP knockout (KO) mice to generate Rip1-Tag2;SAP-/- mice. We found that SAP deletion significantly promoted the growth, invasion and metastasis of malignant insulinoma through C-X-C motif chemokine ligand 12 (CXCL12) secreted by cancer-associated fibroblasts (CAFs). Further study showed that SAP deletion promoted CXCL12 secretion by CAFs through the CXCR4/p38/ERK signalling pathway. These findings reveal a novel role and mechanism of SAP in malignant insulinoma and provide direct evidence that SAP may be a therapeutic agent for this disease.

Cigarette Smoke Extract-Treated Mouse Airway Epithelial Cells-Derived Exosomal LncRNA MEG3 Promotes M1 Macrophage Polarization and Pyroptosis in Chronic Obstructive Pulmonary Disease by Upregulating TREM-1 via m6A Methylation.

Cigarette smoke extract (CSE)-treated mouse airway epithelial cells (MAECs)-derived exosomes accelerate the progression of chronic obstructive pulmonary disease (COPD) by upregulating triggering receptor expressed on myeloid cells 1 (TREM-1); however, the specific mechanism remains unclear. We aimed to explore the potential mechanisms of CSE-treated MAECs-derived exosomes on M1 macrophage polarization and pyroptosis in COPD. In vitro, exosomes were extracted from CSE-treated MAECs, followed by co-culture with macrophages. In vivo, mice exposed to cigarette smoke (CS) to induce COPD, followed by injection or/and intranasal instillation with oe-TREM-1 lentivirus. Lung function and pathological changes were evaluated. CD68+ cell number and the levels of iNOS, TNF-α, IL-1ß (M1 macrophage marker), and pyroptosis-related proteins (NOD-like receptor family pyrin domain containing 3, apoptosis-associated speck-like protein containing a caspase-1 recruitment domain, caspase-1, cleaved-caspase-1, gasdermin D [GSDMD], and GSDMD-N) were examined. The expression of maternally expressed gene 3 (MEG3), spleen focus forming virus proviral integration oncogene (SPI1), methyltransferase 3 (METTL3), and TREM-1 was detected and the binding relationships among them were verified. MEG3 increased N6-methyladenosine methylation of TREM-1 by recruiting SPI1 to activate METTL3. Overexpression of TREM-1 or METTL3 negated the alleviative effects of MEG3 inhibition on M1 polarization and pyroptosis. In mice exposed to CS, EXO-CSE further aggravated lung injury, M1 polarization, and pyroptosis, which were reversed by MEG3 inhibition. TREM-1 overexpression negated the palliative effects of MEG3 inhibition on COPD mouse lung injury. Collectively, CSE-treated MAECs-derived exosomal long non-coding RNA MEG3 may expedite M1 macrophage polarization and pyroptosis in COPD via the SPI1/METTL3/TREM-1 axis.

Identification and characterization of novel genetic variants in the first Chinese family of mucopolysaccharidosis IIIC (Sanfilippo C syndrome).

Mucopolysaccharidosis type IIIC (MPS IIIC) is one of inherited lysosomal storage disorders, caused by deficiencies in lysosomal hydrolases degrading acidic mucopolysaccharides. The gene responsible for MPS IIIC is HGSNAT, which encodes an enzyme that catalyses the acetylation of the terminal glucosamine residues of heparan sulfate. So far, few studies have focused on the genetic landscape of MPS IIIC in China, where IIIA and IIIB were the major subtypes. In this study, we utilized whole-exome sequencing (WES) to identify novel compound heterozygous variants in the HGSNAT gene from a Chinese patient with typical MPS IIIC symptoms: c.743G>A; p.Gly248Glu and c.1030C>T; p.Arg344Cys. We performed in silico analysis and experimental validation, which confirmed the deleterious pathogenic nature of both variants, as evidenced by the loss of HGSNAT activity and failure of lysosomal localization. To the best of our knowledge, the MPS IIIC is first confirmed by clinical, biochemical and molecular genetic findings in China. Our study thus expands the spectrum of MPS IIIC pathogenic variants, which is of importance to dissect the pathogenesis and to carry out clinical diagnosis of MPS IIIC. Moreover, this study helps to depict the natural history of Chinese MPS IIIC populations.

Sleep-dependent engram reactivation during hippocampal memory consolidation associated with subregion-specific biosynthetic changes.

Post-learning sleep is essential for hippocampal memory processing, including contextual fear memory consolidation. We labeled context-encoding engram neurons in the hippocampal dentate gyrus (DG) and assessed reactivation of these neurons after fear learning. Post-learning sleep deprivation (SD) selectively disrupted reactivation of inferior blade DG engram neurons, linked to SD-induced suppression of neuronal activity in the inferior, but not superior DG blade. Subregion-specific spatial profiling of transcripts revealed that transcriptomic responses to SD differed greatly between hippocampal CA1, CA3, and DG inferior blade, superior blade, and hilus. Activity-driven transcripts, and those associated with cytoskeletal remodeling, were selectively suppressed in the inferior blade. Critically, learning-driven transcriptomic changes differed dramatically between the DG blades and were absent from all other regions. Together, these data suggest that the DG is critical for sleep-dependent memory consolidation, and that the effects of sleep loss on the hippocampus are highly subregion-specific.

EPAC inhibitor suppresses angiogenesis and tumor growth of triple-negative breast cancer.

AIMS: Exchange protein directly activated by cAMP 1 (EPAC1), a major isoform of guanine nucleotide exchange factors, is highly expressed in vascular endothelia cells and regulates angiogenesis in the retina. High intratumor microvascular densities (MVD) resulting from angiogenesis is responsible for breast cancer development. Downregulation of EPAC1 in tumor cell reduces triple-negative breast cancer (TNBC)-induced angiogenesis. However, whether Epac1 expressed in vascular endothelial cells contributes to angiogenesis and tumor development of TNBC remains elusive. MAIN METHODS: We employed NY0123, a previously identified potent EPAC inhibitor, to explore the anti-angiogenic biological role of EPAC1 in vitro and in vivo through vascular endothelial cells, rat aortic ring, Matrigel plug, and chick embryo chorioallantoic membrane (CAM) and yolk sac membrane (YSM) assays, as well as the in vivo xenograft tumor models of TNBC in both chick embryo and mice. KEY FINDINGS: Inhibiting EPAC1 in vascular endothelial cells by NY0123 significantly suppresses angiogenesis and tumor growth of TNBC. In addition, NY0123 possesses a better inhibitory efficacy than ESI-09, a reported specific EPAC inhibitor tool compound. Importantly, inhibiting EPAC1 in vascular endothelia cells regulates the typical angiogenic signaling network, which is associated with not only vascular endothelial growth factor (VEGF)/vascular endothelial growth factor receptor-2 (VEGFR2) signaling, but also PI3K/AKT, MEK/ERK and Notch pathway. CONCLUSIONS: Our findings support that EPAC1 may serve as an effective anti-angiogenic therapeutic target of TNBC, and EPAC inhibitor NY0123 has the therapeutic potential to be developed for the treatment of TNBC.

Relationships between Motor Skills and Academic Achievement in School-Aged Children and Adolescents: A Systematic Review.

PURPOSE: This review systematically summarizes the studies of the relationship between primary-to-secondary school students' motor skills and academic achievement, and analyzes the relationship between gross and fine motor skills and performance in different subjects. METHOD: Five electronic databases, Web Of Science, PubMed, PsycINFO, SPORTDiscus, and Academic Search Premier, were searched in March 2023. Semi-quantitative assessment methods were used to analyze the results of the included studies. RESULTS: Seventy-eight articles were included in this systematic review. The semi-quantitative assessment results showed that gross (+, 65.0/62.5%) and fine motor skills (+, 83.3/80%) were positively correlated with overall performance and language performance, with ≥60% of the associations in the same direction. For different subjects, fine motor skills were positively correlated with students' mathematics (+, 75.0%), reading (+, 72.7%), writing (+, 66.7%), and spelling (+, 60.0%) scores. However, the association between gross motor skills and students' mathematics achievement (?, 52.8%), reading (?, 53.8%), and spelling (?, 50.0%) is uncertain, with <60% of the associations in the same direction. CONCLUSIONS: It is wise to direct our gaze toward the evolution of motor skills among students, especially primary school students. Different motor skill intervention modes should be selected in a targeted manner according to different subject achievements.

Near-full-length genome analysis of two novel HIV second recombinant forms in Hebei, China.

The number of individuals infected with HIV-1 among men who have sex with men (MSM) has risen rapidly in recent years in China, and the subtypes CRF01_AE, CRF07_BC, and B, as well as many novel unique recombinant forms (URFs) are prevalent among them. Co-circulation of strains among MSM populations allows the generation of circulating recombinant forms (CRFs) and URFs. In this study, we identified two new URFs from two HIV-1-positive subjects who were infected through homosexual contact in Hebei, China. Analysis of near-full-length genome sequences, using phylogenetic and recombination analysis showed that the two URFs originated from CRF01_AE, CRF07_BC, and B, and CRF01_AE segments in the backbone of the URFs were derived from cluster 4 of CRF01_AE. The CRF07_BC segments of two URFs were clustered with 07BC_N in a phylogenetic tree. The identification of novel URFs with complex genomic structures shows that it is necessary to strengthen surveillance of HIV-1 variants in MSM populations in this region.