Circ_0021155 can participate in the phenotypic transformation of human vascular smooth muscle cells via the miR-4459/TRPM7 axis.

The phenotypic transformation of vascular smooth muscle cells (VSMCs) plays a key role in the pathological process of atherosclerosis (AS), and TRPM7 is involved in this process. In this study, we verified whether circRNAs participate in the phenotypic transformation of VSMCs by regulating TRPM7 in AS. The RNA-sequencing data of atherosclerosis were downloaded and analysed from the GEO database. Only hsa_circ_0021155 related to TRPM7 was differentially expressed in AS. circRNA distribution and expression were observed via FISH and PCR. CCK8, scratch test and Transwell assay were used to observe the proliferation and migration of cells. Western blot was performed to examine changes in α-actin, calponin, SMMHC and TRPM7 proteins. The expression of hsa_circ_0021155 against has-miR-4459/miR-3689c was verified via PCR. The ceRNA relationship of TPRM7-miR4459-circ0021155 was verified via dual luciferase assay, and the effects of miR4459 mimic/inhibitor on the proliferation of cells were further observed. The expression of hsa_circ_0021155 and OX-LDL was increased in VSMCs. hsa_circ_0021155 promoted the expression of TRPM7 and inhibited the protein expression of α-actin, calponin and SMMHC. In addition, it promoted the proliferation and migration of cells and inhibited the expression of miR-3689c and miR-4459 but did not affect miR-4756-5p. The dual luciferase assay showed that circ0021155-miR4459-TRPM7 mRNA was highly compatible and could be mutually regulated by a ceRNA network. In conclusion, hsa_circ_0021155 regulates the proliferation, migration and phenotype transformation of VSMCs induced by OX-LDL via the miR-4459/TRPM7 axis. hsa_circ_0021155 and TRPM7 may offer novel therapeutic targets for atherosclerosis.

Maize kernel development.

Maize (Zea mays) is a leading cereal crop in the world. The maize kernel is the storage organ and the harvest portion of this crop and is closely related to its yield and quality. The development of maize kernel is initiated by the double fertilization event, leading to the formation of a diploid embryo and a triploid endosperm. The embryo and endosperm are then undergone independent developmental programs, resulting in a mature maize kernel which is comprised of a persistent endosperm, a large embryo, and a maternal pericarp. Due to the well-characterized morphogenesis and powerful genetics, maize kernel has long been an excellent model for the study of cereal kernel development. In recent years, with the release of the maize reference genome and the development of new genomic technologies, there has been an explosive expansion of new knowledge for maize kernel development. In this review, we overviewed recent progress in the study of maize kernel development, with an emphasis on genetic mapping of kernel traits, transcriptome analysis during kernel development, functional gene cloning of kernel mutants, and genetic engineering of kernel traits.

Maize endosperm development.

Recent breakthroughs in transcriptome analysis and gene characterization have provided valuable resources and information about the maize endosperm developmental program. The high temporal-resolution transcriptome analysis has yielded unprecedented access to information about the genetic control of seed development. Detailed spatial transcriptome analysis using laser-capture microdissection has revealed the expression patterns of specific populations of genes in the four major endosperm compartments: the basal endosperm transfer layer (BETL), aleurone layer (AL), starchy endosperm (SE), and embryo-surrounding region (ESR). Although the overall picture of the transcriptional regulatory network of endosperm development remains fragmentary, there have been some exciting advances, such as the identification of OPAQUE11 (O11) as a central hub of the maize endosperm regulatory network connecting endosperm development, nutrient metabolism, and stress responses, and the discovery that the endosperm adjacent to scutellum (EAS) serves as a dynamic interface for endosperm-embryo crosstalk. In addition, several genes that function in BETL development, AL differentiation, and the endosperm cell cycle have been identified, such as ZmSWEET4c, Thk1, and Dek15, respectively. Here, we focus on current advances in understanding the molecular factors involved in BETL, AL, SE, ESR, and EAS development, including the specific transcriptional regulatory networks that function in each compartment during endosperm development.

Maize pentatricopeptide repeat protein DEK53 is required for mitochondrial RNA editing at multiple sites and seed development.

Pentatricopeptide repeat (PPR) proteins were identified as site-specific recognition factors for RNA editing in plant mitochondria and plastids. In this study, we characterized maize (Zea mays) kernel mutant defective kernel 53 (dek53), which has an embryo lethal and collapsed endosperm phenotype. Dek53 encodes an E-subgroup PPR protein, which possesses a short PLS repeat region of only seven repeats. Subcellular localization analysis indicated that DEK53 is localized in the mitochondrion. Strand- and transcript-specific RNA-seq analysis showed that the dek53 mutation affected C-to-U RNA editing at more than 60 mitochondrial C targets. Biochemical analysis of mitochondrial protein complexes revealed a significant reduction in the assembly of mitochondrial complex III in dek53. Transmission electron microscopic examination showed severe morphological defects of mitochondria in dek53 endosperm cells. In addition, yeast two-hybrid and luciferase complementation imaging assays indicated that DEK53 can interact with the mitochondrion-targeted non-PPR RNA editing factor ZmMORF1, suggesting that DEK53 might be a functional component of the organellar RNA editosome.

Maize Dek33 encodes a pyrimidine reductase in riboflavin biosynthesis that is essential for oil-body formation and ABA biosynthesis during seed development.

The maize (Zea mays) defective kernel 33 (dek33) mutant produces defective and occasionally viviparous kernel phenotypes. In this study, we cloned Dek33 by positional cloning and found that it encodes a pyrimidine reductase in riboflavin biosynthesis. In dek33, a single-base mutation (G to A) in the C-terminal COG3236 domain caused a premature stop codon (TGA), producing a weak mutant allele with only a truncated form of the DEK33 protein that occurred at much lower levels that the completed WT form, and with a reduced riboflavin content. The dek33 mutation significantly affected oil-body formation and suppressed endoreduplication. It also disrupted ABA biosynthesis, resulting in lower ABA content that might be responsible for the viviparous embryo. In addition, our results indicated that the COG3236 domain is important for the protein stability of DEK33. Yeast two-hybrid experiments identified several proteins that interacted with DEK33, including RGLG2 and SnRK1, suggesting possible post-translational regulation of DEK33 stability. The interaction between DEK33 and these proteins was further confirmed by luciferase complementation image assays. This study provides a weak mutant allele that can be utilized to explore cellular responses to impaired riboflavin biosynthesis during seed development. Our findings indicate that the COG3236 domain might be an essential regulatory structure for DEK33 stability in maize.

Inhibition of Cyclin D1 Expression in Human Glioblastoma Cells is Associated with Increased Temozolomide Chemosensitivity.

BACKGROUND/AIMS: Cyclin D1 (CCND1) is frequently overexpressed in malignant gliomas. We have previously shown ectopic overexpression of CCND1 in human malignant gliomas cell lines. METHODS: Quantitative reverse transcriptase PCR (qRT-PCR) and Western Blot (WB) was performed to investigate the expression of CCND1 in glioma tissues and cell lines. The biological function of CCND1 was also investigated through knockdown and overexpression of BCYRN1 in vitro. RESULTS: Here we reported that CCND1 expression was positively associated with the pathological grade and proliferative activity of astrocytomas, as the lowest expression was found in normal brain tissue (N = 3) whereas the highest expression was in high-grade glioma tissue (N = 25). Additionally, we found that the expression level of CCND1 was associated with IC50 values in malignant glioma cell lines. Forced inhibition of CCND1 increased temozolomide efficacy in U251 and SHG-44 cells. After CCND1 overexpression, the temozolomide efficacy decreased in U251 and SHG-44 cells. Colony survival assay and apoptosis analysis confirmed that CCND1 inhibition renders cells more sensitive to temozolomide treatment and temozolomide-induced apoptosis in U251 and SHG-44 cells. Inhibition of P-gp (MDR1) by Tariquidar overcomes the effects of CCND1 overexpression on inhibiting temozolomide-induced apoptosis. Inhibition of CCND1 inhibited cell growth in vitro and in vivo significantly more effectively after temozolomide treatments than single temozolomide treatments. Finally, inhibition of CCND1 in glioma cells reduced tumor volume in a murine model. CONCLUSION: Taken together, these data indicate that CCND1 overexpression upregulate P-gp and induces chemoresistance in human malignant gliomas cells and that inhibition of CCND1 may be an effective means of overcoming CCND1 associated chemoresistance in human malignant glioma cells.

Sphingosine kinase 1/sphingosine-1-phosphate regulates the expression of interleukin-17A in activated microglia in cerebral ischemia/reperfusion.

BACKGROUND: Microglial activation is one of the causative factors of neuroinflammation in cerebral ischemia/reperfusion (IR). Sphingosine kinase 1 (Sphk1), a key enzyme responsible for phosphorylating sphingosine into sphingosine-1-phosphate (S1P), plays an important role in the regulation of proinflammatory cytokines in activated microglia. Recent research demonstrated that S1P increased IL-17A-secretion and then worsened CNS (central nervous system) inflammation. Thus, in the present study, we sought to use microglial cells as the object of study to discuss the molecular mechanisms in Sphk1/S1P-regulated IL-17A-secretion in IR. METHODS: We used immunofluorescence and confocal microscopy to detect whether Sphk1 is expressed in microglia after cerebral IR or oxygen-glucose deprivation (OGDR). Western blot analysis was used to estimate the total Sphk1 protein level at different time points after OGDR. To detect cytokine secretion in microglial supernatants in response to OGDR, we measured the concentration of IL-17A in the culture supernatants using an enzyme-linked immunosorbent assay (ELISA). To evaluate whether microglia subjected to OGDR exhibited neuronal injury, we used a commercially available terminal transferase-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) kit to detect apoptotic neurons. RESULTS: Sphk1 was expressed in microglia in response to cerebral IR or OGDR at appointed time. Pre-injection with PF-543, an inhibitor of Sphk1, before IR clearly reduced the expression of Sphk1 in microglia relative to brain IR alone. The number of TUNEL-positive neurons was also decreased in the PF-543-pretreated animals before IR compared to the animals with IR alone. When S1P was administered in OGDR microglia, IL-17A expression and neuronal apoptosis were increased compared to OGDR alone and the administration of S1P alone. ELISA further confirmed the above results. Moreover, the inhibition of Sphk1 by siRNA reduced IL-17A production and relieved neuronal apoptosis in OGDR microglia. CONCLUSION: These results indicated that Sphk1/S1P regulates the expression of IL-17A in activated microglia, inducing neuronal apoptosis in cerebral ischemia/reperfusion. The microglial Sphk1/S1P pathway may thus be a potential therapeutic target to control neuroinflammation in brain IR.

Expression of NF-κB, MCP-1 and MMP-9 in a Cerebral Aneurysm Rabbit Model.

OBJECTIVE: We explored the early expression of NF-κB, MCP-1 and -MMP 9 in a rabbit carotid aneurysm model, and investigated the possible mechanism of aneurysm. METHODS: twenty four adult new Zealand rabbits were divided into four groups. normal control (group a); rabbits received elastase induction for 1, 2 3 weeks (group b, C and d respectively); hematoxylin-eosin stains were performed for observation. the mrna and protein expression of NF-κB, MCP-1 and MMP-9 were analyzed using RT-PCR and immunohistochemical methods. RESULTS: the expression of NF-κB and MCp-1 reached their peaks after induction for one week, then decreased. their expression in week 1 and week 2 had no statistical difference. the expression of MMP-9 increased after induction. We observed the highest expression at week 3. as the induction time increased, the number of smooth muscles reduced. endothelial cells were damaged; the aneurysm wall elastic layer was damaged. CONCLUSION: activation of NF-κB may be one of the initiating factors contributing to the occurrence and development of cerebral aneurysm. MCP-1 induced macrophage adhesion and infiltration in the artery wall of cerebral aneurysms, and contributed to the occurrence and development of brain aneurysm. damage to elastic fibers is one of the key factors for aneurysm formation. increased infiltration of inflammatory cells and the secretion of MMP-9 are the main reasons for elastic fiber damage.

Distinct roles of neuregulin in different models of neuropathic pain.

The objective of the study was to investigate the role of neuregulin-ErbB signaling in neuropathic pain in different types of injury. Neuregulin-1(NRG-1) was injected into animals with either formalin-induced pain model or spared nerve injury (SNI) model. Formalin tests or paw withdrawal tests were performed to study the role of NRG-1 in neuropathic pain. siRNA specific to different erbB receptors were then introduced to test which specific signaling pathway was required for NRG-1 signaling in the different pain models. NRG-1 inhibits neuropathic pain after SNI in a dose-dependent manner, while NRG-1 aggravates formalin-induced neuropathic pain. ErbB2 and erbB4 receptors were activated after neuregulin administration. Knockdown of ErbB2 relieves the aggravation of NRG-1 on formalin-induced neuropathic pain, and knockdown of ErbB4 could relieve the inhibition of NRG-1 on neuropathic pain in the SNI model. NRG-1 has two distinct functions depending on the different receptor activation in different models of neuropathic pain. These novel findings may provide new therapeutic approaches for the treatment of neuropathic pain in different injury types.

Efficacy of neuroendoscopic-assisted surgery in the management of symptomatic sacral perineural (Tarlov) cysts: a technical report.

Introduction: The Tarlov cysts are pathological enlargements of the cerebrospinal fluid spaces between the endoneurium and perineurium, which can cause intolerable sciatic pain, motor impairment of lower limbs, and bladder/bowel dysfunction. Currently, the treatment results are unsatisfactory due to the low cure rates and extensive surgical trauma. Thus, there is an ongoing exploration of surgical techniques for Tarlov treatment. In the current study, we present a novel neuroendoscopic-assisted technique that combines the fenestration, leakage sealing, and tamponade of the Tarlov cyst. Methods: Between January 2020 and December 2021, a total of 32 Tarlov patients were enrolled and received neuroendoscopic-assisted surgery. Their pre- and post-surgical Visual Analogue Scale (VAS) scores, major complaints, and MR imaging were recorded for comparison. Results: 27 of 32 patients (84.4%) patients demonstrated immediate pain relief as their VAS scores decreased from 5.6 ± 1.5 to 2.5 ± 1.1 (p < 0.01) on the first day after surgery. At the 3-month follow-up, the patients' average VAS score continued to decrease (1.94 ± 0.8). Meanwhile, saddle paresthesia, urinary incontinence, and constipation were relieved in 6 (50%), 4 (80%), and 5 (41.7%), respectively, according to patients self-report. No surgical-related complication was observed in any of the cases. Discussion: We conclude that neuroendoscopic-assisted surgery is an effective surgical method for symptomatic Tarlov cysts with minimized complications.

Syringo-Subarachnoid Shunt with Tube Versus T-Tube via the Dorsal Root Entry Zone Approach for Eccentric Syringomyelia.

OBJECTIVE: This study compared the clinical therapeutic efficacy of syringo-subarachnoid shunt placement with direct tube and T-tube via the dorsal root entry zone (DREZ) approach for treatment of eccentric syringomyelia. METHODS: A retrospective study was performed of 41 patients with idiopathic or secondary eccentric syringomyelia from November 2011 to December 2022. Syringo-subarachnoid shunt placement with direct tube or T-tube via the DREZ approach was performed. The modified Japanese Orthopaedic Association low back pain scale was used to investigate the severity of clinical symptoms. Magnetic resonance imaging was used to investigate therapeutic efficacy（reduction of the cavity volume by >10% was considered an improvement and 50% was considered a significant improvement). RESULTS: Incision length of the spinal cortex in the direct tube group was shorter than in the T-tube group (3.10 ± 0.28 cm vs. 5.03 ± 0.19 cm), with a significant difference between the 2 groups (t = -52.56, P < 0.001). Modified Japanese Orthopaedic Association score 3 months postoperatively was significantly better than the preoperative score in both the direct tube group（t = 40.954, P < 0.001） and the T-tube group（t = 24.769, P < 0.001）. Statistical comparison revealed there was no difference in imaging improvement between the direct tube group and T-tube group 3 months (χ2 = 0.20, P = 0.655) and 12 months (χ2 = 0.21, P = 0.647) postoperatively. CONCLUSIONS: Syringo-subarachnoid shunt placement with direct tube via the DREZ approach for treatment of eccentric syringomyelia is safer than with T-tube via the DREZ approach due to smaller incision length and less of a space-occupying effect with same therapeutic efficacy.

Research on industrial carbon emission prediction and resistance analysis based on CEI-EGM-RM method: a case study of Bengbu.

This paper focuses on the development trend of industrial carbon emissions in Bengbu city, Anhui Province in the next ten years, and how to help the industry reach the carbon peak as soon as possible. The research process and conclusions are as follows: (1) Through literature review and carbon emission index method, five main factors affecting industrial carbon emission are identified. (2) The resistance model is used to analyze the main resistance factors of industrial carbon emission reduction in Bengbu city. (3) Based on the existing data of Bengbu city from 2011 to 2020, the grey prediction EGM (1,1) model is used to predict the industrial carbon emissions of Bengbu city from 2021 to 2030. The results show that among the five factors, the urbanization rate has the most significant impact on industrial carbon emissions, while energy intensity has the least impact. Bengbu's industrial carbon emissions will continue to increase in the next decade, but the growth rate will be flat. Based on the findings of the analysis, specific recommendations on urbanization development, energy structure, and industrial structure of Bengbu city are put forward.

Identification of MPK4 interacting proteins in guard cells.

Plants as sessile organisms are challenged by numerous biotic and abiotic stresses. Stomatal guard cells on the leaf surface are at the frontline of biotic and abiotic stress responses. Mitogen-activated protein kinase 4 (MPK4) has higher expression levels in guard cells than in mesophyll cells. The specific functions of MPK4 in guard cells are unknown. In this study, when MPK4 was overexpressed in Arabidopsis, bacterial entry of Pseudomonas syringae (Pst) into the plants was significantly decreased. The MPK4 overexpression plants had a similar trend of stomatal movement as wild-type Col-0, but had a smaller stomatal aperture than the Col-0, highlighting MPK4 plays a role in stomatal immune response. This function of the MPK4 requires its kinase activity because the MPK4 kinase-dead mutant did not have a significant difference in stomatal aperture compared to the Col-0. To understand MPK4 functions in guard cells, we investigated MPK4-associated protein complexes in guard cells using affinity purification mass spectrometry. A total of 145 proteins were identified to be in the MPK4-complex. Ten potential MPK4-interacting proteins were cloned and tested for physical interactions with the MPK4 using a yeast two hybrid (Y2H) system. Four proteins were newly identified to interact directly with the MPK4. SIGNIFICANCE: MPK4 is highly abundant in stomatal guard cells, but its specific functions in guard cells are largely unknown. Through a bacterial entry assay of MPK4 overexpression plants, we found that MPK4 may play an important role in stomatal immune response. To understand the molecular mechanisms underlying the MPK4 functions in guard cells, we characterized the MPK4-associated protein complex in guard cells. Many of the 145 identified proteins were involved in plant immunity and development. Four of the proteins were newly identified to interact directly with the MPK4. This work has provided additional evidence for the MPK4 function as a positive regulator for stomatal immunity. The guard cell MPK4 protein complex and the four new interacting proteins were revealed. Whether MPK4 directly phosphorylates these interacting proteins deserves further investigation. These newly discovered proteins have chartered exciting directions toward understanding new functions of the MPK4 kinase.

Dynamic DNA methylation turnover in gene bodies is associated with enhanced gene expression plasticity in plants.

BACKGROUND: In several eukaryotes, DNA methylation occurs within the coding regions of many genes, termed gene body methylation (GbM). Whereas the role of DNA methylation on the silencing of transposons and repetitive DNA is well understood, gene body methylation is not associated with transcriptional repression, and its biological importance remains unclear. RESULTS: We report a newly discovered type of GbM in plants, which is under constitutive addition and removal by dynamic methylation modifiers in all cells, including the germline. Methylation at Dynamic GbM genes is removed by the DRDD demethylation pathway and added by an unknown source of de novo methylation, most likely the maintenance methyltransferase MET1. We show that the Dynamic GbM state is present at homologous genes across divergent lineages spanning over 100 million years, indicating evolutionary conservation. We demonstrate that Dynamic GbM is tightly associated with the presence of a promoter or regulatory chromatin state within the gene body, in contrast to other gene body methylated genes. We find Dynamic GbM is associated with enhanced gene expression plasticity across development and diverse physiological conditions, whereas stably methylated GbM genes exhibit reduced plasticity. Dynamic GbM genes exhibit reduced dynamic range in drdd mutants, indicating a causal link between DNA demethylation and enhanced gene expression plasticity. CONCLUSIONS: We propose a new model for GbM in regulating gene expression plasticity, including a novel type of GbM in which increased gene expression plasticity is associated with the activity of DNA methylation writers and erasers and the enrichment of a regulatory chromatin state.

Paternal imprinting of dosage-effect defective1 contributes to seed weight xenia in maize.

Historically, xenia effects were hypothesized to be unique genetic contributions of pollen to seed phenotype, but most examples represent standard complementation of Mendelian traits. We identified the imprinted dosage-effect defective1 (ded1) locus in maize (Zea mays) as a paternal regulator of seed size and development. Hypomorphic alleles show a 5-10% seed weight reduction when ded1 is transmitted through the male, while homozygous mutants are defective with a 70-90% seed weight reduction. Ded1 encodes an R2R3-MYB transcription factor expressed specifically during early endosperm development with paternal allele bias. DED1 directly activates early endosperm genes and endosperm adjacent to scutellum cell layer genes, while directly repressing late grain-fill genes. These results demonstrate xenia as originally defined: Imprinting of Ded1 causes the paternal allele to set the pace of endosperm development thereby influencing grain set and size.

A functional p.82G>S polymorphism in the RAGE gene is associated with multiple sclerosis in the Chinese population.

BACKGROUND: The receptor for advanced glycation end products (RAGE) and its proinflammatory ligand, S100-calgranulins, are critically implicated in the pathological progression of multiple sclerosis (MS). A functional polymorphism within the V-type immunoglobulin domain of RAGE gene, p.82G>S (c.557G>A), has been shown to affect ligand binding affinity and thus may affect susceptibility to MS. METHODS: The RAGE p.82G>S polymorphism was genotyped in 144 MS patients and 156 healthy controls using polymerase chain reaction - restriction fragment length polymorphism. A replication study was performed on a second cohort comprising 138 patients and 150 controls. The relationship between the RAGE p.82G>S polymorphism and circulating levels of soluble RAGE (sRAGE), a secreted decoy receptor against RAGE signaling, was also investigated. RESULTS: In both initial and replication cohorts, an increased MS risk was detected in RAGE p.82G>S variant allele carriers (odds ratio [OR] = 1.786, p = 0.0134 and OR = 1.732, p = 0.0210, respectively). This association signal persisted in subgroups of women and patients with relapsing-remitting MS. Moreover, compared with the wild-type 82GG carriers, carriers of the variant allele presented a faster progression of disability and a reduced serum sRAGE level. CONCLUSIONS: The present study provides preliminary evidence that the gain-of-function p.82G>S polymorphism in the RAGE gene is associated with an increased risk of MS in the Chinese population.

Association between the RAGE G82S polymorphism and Alzheimer's disease.

The receptor for advanced glycation end products (RAGE) is associated with several pathological states including Alzheimer's disease (AD) pathology, while its soluble form (sRAGE) acts as a decoy receptor. We have tested for association of AD with a functional single-nucleotide polymorphism (SNP) in the RAGE gene (G82S; rs2070600), a SNP associated with increased ligand affinity of RAGE. Analysis of a Chinese cohort (276 cases; 254 controls) showed a higher prevalence of the RAGE 82S allele and GS + SS genotype in the patients [82S vs. 82G: P = 0.017, odds ratio (OR) = 1.431; GS + SS vs. GG: P = 0.025, OR = 1.490]. Further stratification analysis revealed that the association of the RAGE G82S polymorphism with AD was significant in early onset AD stratum. Moreover, plasma sRAGE levels were lower in AD than in normal elderly controls, and the presence of the risk allele was associated with further plasma sRAGE reduction and a fast cognitive deterioration. The present study provides preliminary evidence that the RAGE G82S variant is involved in genetic susceptibility to AD.

Air pollution and temperature are associated with increased COVID-19 incidence: A time series study.

OBJECTIVES: Although COVID-19 is known to be caused by human-to-human transmission, it remains largely unclear whether ambient air pollutants and meteorological parameters could promote its transmission. METHODS: A retrospective study was conducted to study whether air quality index (AQI), four ambient air pollutants (PM2.5, PM10, NO2 and CO) and five meteorological variables (daily temperature, highest temperature, lowest temperature, temperature difference and sunshine duration) could increase COVID-19 incidence in Wuhan and XiaoGan between Jan 26th to Feb 29th in 2020. RESULTS: First, a significant correlation was found between COVID-19 incidence and AQI in both Wuhan (R2=0.13, p<0.05) and XiaoGan (R2=0.223, p<0.01). Specifically, among four pollutants, COVID-19 incidence was prominently correlated with PM2.5 and NO2 in both cities. In Wuhan, the tightest correlation was observed between NO2 and COVID-19 incidence (R2=0.329, p<0.01). In XiaoGan, in addition to the PM2.5 (R2=0.117, p<0.01) and NO2 (R2=0.015, p<0.05), a notable correlation was also observed between the PM10 and COVID-19 incidence (R2=0.105, p<0.05). Moreover, temperature is the only meteorological parameter that constantly correlated well with COVID-19 incidence in both Wuhan and XiaoGan, but in an inverse correlation (p<0.05). CONCLUSIONS: AQI, PM2.5, NO2, and temperature are four variables that could promote the sustained transmission of COVID-19.

Interaction between interleukin-8 and methylenetetrahydrofolate reductase genes modulates Alzheimer's disease risk.

BACKGROUND/AIM: Interleukin-8 (IL-8), a potent chemoattractant for neutrophils, has been implicated in the pathogenesis of Alzheimer's disease (AD). The ability of individuals to produce high levels of IL-8 is partially determined by the IL-8 -251 T/A polymorphism. Therefore, we investigated the association between this polymorphism and AD in a Chinese population. Additionally, in light of the stimulatory effect of homocysteine on the production of IL-8, we also sought to determine whether the methylenetetrahydrofolate reductase (MTHFR) gene 677 C/T variant, a genetic modifier of the serum homocysteine level, may interact with the IL-8 -251 polymorphism in determining the AD risk. METHODS: Genotyping of 198 AD patients and 240 matched controls was performed by PCR-RFLP. RESULTS: The presence of the MTHFR 677 C/T and 677 T/T genotypes conferred a marginally significant increase in the risk for AD (OR = 1.666, 95% CI = 1.022-2.715, and OR = 1.892, 95% CI = 1.124-3.187) and the presence of the IL-8 -251 polymorphism was not associated with AD. However, the OR for AD associated with joint occurrence of the MTHFR 677 T/T and the IL-8 -251 A/A genotypes was 2.512 (95% CI = 1.151-5.483). CONCLUSION: Our data suggest a critical role for IL-8/MTHFR interactions in the development of AD.

Posterior reversible encephalopathy syndrome with spinal cord involvement but without hemisphere lesions: A case report.

RATIONALE: Posterior reversible encephalopathy syndrome (PRES) was termed by Hinchey in 1996. Patients have a reversible vasogenic brain edema in imaging and acute neurological symptoms such as headache, seizures, encephalopathy, and visual disturbances when suffering from hypertension, pre-eclampsia/eclampsia, renal failure, immunosuppressive medications, autoimmune disorders, sepsis, thrombocytopaenia, hypocalcaemia, alcohol withdrawal, and many other potential causes. de Havenon A et al have proposed a new syndrome named PRES with spinal cord involvement (PRES-SCI). The patients with PRES-SCI have similar symptoms these of PRES. Patients have neurologic signs with the spinal cord involved and lesions in magnetic resonance imaging (MRI) extending to the cervicomedullary junction, usually with extreme elevation in blood pressure and a history of hypertensive retinopathy. We administrated a young patient whose condition was consistent with PRES-SCI except for the hemisphere lesions. PATIENT CONCERNS: A 20-year-old Asian male patient was admitted for a 1 week history of blurred vision and weakness of the limbs. He has had poorly controlled hypertension for 1 year before admission. In emergency room, his blood pressure could raise to 260/140mmHg. Neurological examinations and cerebral spinal fluid tests were negative. The MRI of the brain and spinal cord showed reversible lesions in the medulla and upper cervical spinal cord that extended to the lower thoracic spine. DIAGNOSIS: Taking into account the characteristic lesions in the MRI as well as the reversible course upon treatment, he was diagnosed PRES-SCI. INTERVENTIONS: He was treated with medicines for the hypertension. OUTCOMES: His symptoms rapidly improved and finally the lesions on the MRI of the brain and spianl cord disappeared. LESSONS: Clinicians should suspect PRES-SCI when patients have mild or no neurologic signs accompanied with extreme elevation in blood pressure and lesions in spinal cord. Spinal lesions alone may be a subtype of PRES-SCI.