Acute lung injury (ALI) has been a kind of acute and severe disease that is mainly characterized by systemic uncontrolled inflammatory response to the production of huge amounts of reactive oxygen species (ROS) in the lung tissue. Given the critical role of ROS in ALI, a Fe₃O₄ loaded bovine serum albumin (BSA) nanocluster (BF) was developed to act as a nanomedicine for the treatment of ALI. Combining with NIR irradiation, it exhibited excellent ROS scavenging capacity. Significantly, it also displayed the excellent antioxidant and anti-inflammatory functions for lipopolysaccharides (LPS) induced macrophages (RAW264.7), and Sprague Dawley rats via lowering intracellular ROS levels, reducing inflammatory factors expression levels, inducing macrophage M2 polarization, inhibiting NF-κB signaling pathway, increasing CD4⁺/CD8⁺ T cell ratios, as well as upregulating HSP70 and CD31 expression levels to reprogram redox homeostasis, reduce systemic inflammation, activate immunoregulation, and accelerate lung tissue repair, finally achieving the synergistic enhancement of ALI immunotherapy. It finally provides an effective therapeutic strategy of BF + NIR for the management of inflammation related diseases.

Objective:To investigate the dietary iodine intake of students at Mudanjiang Medical University, Heilongjiang Province.Methods:From September 2023 to June 2024, a two-stage sampling method was used to investigate students at Mudanjiang Medical University. In stage one, 250 students were selected and investigated on their dietary iodine intake using the Iodine Specific Food Frequency Questionnaire (I-FFQ). In stage two, 55 students were selected and the double-meal method was used to investigate the dietary iodine intake of students. Iodine content in food samples was determined by inductively coupled plasma mass spectrometry. Curve estimation (power function, S-shaped curve, cubic equation, growth curve) was applied to analyze the dietary iodine intake of I-FFQ and double-meal method, the regression equation was used to adjust I-FFQ.Results:A total of 237 students were enrolled in I-FFQ, with a dietary iodine intake [ M( Q1, Q3)] of 342.61 (203.77, 399.26) μg/d. The dietary iodine intake of males and females was 361.82 (235.56, 428.98) and 330.87 (190.47, 366.11) μg/d, respectively, and the difference between the two was statistically significant ( Z = - 3.06, P = 0.002). The proportions of insufficient iodine intake, appropriate iodine intake, and excessive iodine intake were 13.92% (33/237), 82.70% (196/237), and 3.38% (8/237), respectively. A total of 52 students were enrolled in the double-meal method, with an average dietary iodine intake of 645.22 (435.91, 960.50) μg/d over 3 days. The proportion of appropriate iodine intake and excessive iodine intake was 44.23% (23/52) and 55.77% (29/52), respectively. After adjusting for I-FFQ, the dietary iodine intake was 650.13 (441.68, 728.53) μg/d, with the proportions of appropriate iodine intake and excessive iodine intake being 35.02% (83/237) and 64.98% (154/237), respectively. Conclusion:More than half of the students at Mudanjiang Medical University in Heilongjiang Province are in a state of excessive iodine intake, and dietary iodine intake should be appropriately controlled.

Objective:To investigate the dietary iodine intake of students at Mudanjiang Medical University, Heilongjiang Province.Methods:From September 2023 to June 2024, a two-stage sampling method was used to investigate students at Mudanjiang Medical University. In stage one, 250 students were selected and investigated on their dietary iodine intake using the Iodine Specific Food Frequency Questionnaire (I-FFQ). In stage two, 55 students were selected and the double-meal method was used to investigate the dietary iodine intake of students. Iodine content in food samples was determined by inductively coupled plasma mass spectrometry. Curve estimation (power function, S-shaped curve, cubic equation, growth curve) was applied to analyze the dietary iodine intake of I-FFQ and double-meal method, the regression equation was used to adjust I-FFQ.Results:A total of 237 students were enrolled in I-FFQ, with a dietary iodine intake [ M( Q1, Q3)] of 342.61 (203.77, 399.26) μg/d. The dietary iodine intake of males and females was 361.82 (235.56, 428.98) and 330.87 (190.47, 366.11) μg/d, respectively, and the difference between the two was statistically significant ( Z = - 3.06, P = 0.002). The proportions of insufficient iodine intake, appropriate iodine intake, and excessive iodine intake were 13.92% (33/237), 82.70% (196/237), and 3.38% (8/237), respectively. A total of 52 students were enrolled in the double-meal method, with an average dietary iodine intake of 645.22 (435.91, 960.50) μg/d over 3 days. The proportion of appropriate iodine intake and excessive iodine intake was 44.23% (23/52) and 55.77% (29/52), respectively. After adjusting for I-FFQ, the dietary iodine intake was 650.13 (441.68, 728.53) μg/d, with the proportions of appropriate iodine intake and excessive iodine intake being 35.02% (83/237) and 64.98% (154/237), respectively. Conclusion:More than half of the students at Mudanjiang Medical University in Heilongjiang Province are in a state of excessive iodine intake, and dietary iodine intake should be appropriately controlled.

Objective:To investigate the relationship between the virulence and the carbapenem resistance phenotype of Klebsiella pneumoniae from blood infection,and to identify carbapenem-resistant and hypervirulent Klebsiella pneumoniae(CR-HVKP)strains.Methods:A total of 192 Klebsiella pneumoniae strains were isolated from blood culture of patients with bloodstream infections from 2016 to 2019,of which 96 isolates were carbapenem-resistant Klebsiella pneumoniae(CRKP)and 96 were carbapenem-sensitive Klebsiella pneumoniae(CSKP).The drug susceptibility was detected by VITEK-2 automatic microbial analyzer;carbapenemase genes,virulence genes and capsule typing were detected by polymerase chain reaction;the high viscosity phenotype of strains was detected by string test,and the genome characteristics of CR-HVKP were detected by whole genome sequencing.Serum killing and biofilm formation test were used to further verify the virulence of CR-HVKP.Results:There were significant differences in drug resistance to common antibiotics,except for minocycline between CSKP and CRKP isolates(all P<0.05).92 out of 96 CRKP isolates carried carbapenemase genes,mainly blaKPC-2.The string tests were positive in 4 isolates of CRKP and 36 isolates of CSKP(P<0.05).The detection rates of virulence genes Kfu,aerobictin,iutA,ybtS,rmpA,magA,allS,and capsule antigen K1 and K2 in CSKP group were significantly higher than those in CRKP group(all P<0.05).One HVKP strain was detected in the CRKP group(CR-HVKP)and 36 HVKP was detected in the CSKP group(P<0.05).The CR-HVKP strain belonged to the MLST412,serotype K57,expressed iutA,entB,mrkD,fimH,and rmpA virulence genes,and showed strong biofilm formation and significantly increased serum resistance.Whole genome sequencing results showed that this CR-HVKP isolate carried blaSHV-145,blaTEM-1,blaCTX-M-3,fosA6,oqxA5,oqxB26,and aac(3)-Ⅱd resistance genes,accompanied by abnormalities in outer membrane protein K(OmpK)35 and OmpK36.Conclusions:The drug resistance of CRKP is significantly higher than that of CSKP,while CRKP carrying fewer virulence genes in both number and types compared to CSKP.A new MLST type of carbapenem-resistant and hypervirulent Klebsiella pneumoniae strain has been detected,which requires clinical awareness and epidemiological monitoring.

As the most common chromosomal disorder compatible to life, Down syndrome (DS) is caused by an extra copy of chromosome 21. Almost all DS patients have cognitive dysfunction. Therefore, it is important to study the underlying pathogenetic mechanism to elucidate its molecular basis. This article has provided a review for the molecular mechanisms of NRIP1 and DYRK1A genes, which have been closely associated with the cognitive dysfunctions of DS patients. It has also summarized the research progress on the mechanism of DS and development of new therapeutic strategies based on such studies, with an aim to provide insights into the prevention and treatment for the cognitive dysfunctions in DS patients.
Down Syndrome/psychology* ; Humans ; Protein-Tyrosine Kinases/genetics* ; Dyrk Kinases ; Protein Serine-Threonine Kinases/genetics* ; Cognition Disorders/etiology*

As the most common chromosomal disorder compatible to life, Down syndrome (DS) is caused by an extra copy of chromosome 21. Almost all DS patients have cognitive dysfunction. Therefore, it is important to study the underlying pathogenetic mechanism to elucidate its molecular basis. This article has provided a review for the molecular mechanisms of NRIP1 and DYRK1A genes, which have been closely associated with the cognitive dysfunctions of DS patients. It has also summarized the research progress on the mechanism of DS and development of new therapeutic strategies based on such studies, with an aim to provide insights into the prevention and treatment for the cognitive dysfunctions in DS patients.

Objective To investigate the clinical characteristics and molecular epidemiology of carbapenem-resistant Klebsiella pneumoniae(CRKP)isolated from patients with bloodstream infections in a large tertiary-care general hospital in Southwest China.Methods A total of 131 strains of non-repeating CRKP were collected from the blood cultures of patients who had bloodstream infections in 2015-2019.The strains were identified by VITEK-2,a fully automated microbial analyzer,and matrix-assisted laser desorption ionization-time of flight(MALDI-TOF)mass spectrometry.The minimum inhibitory concentration(MIC)was determined by microbroth dilution method.The common carbapenemase resistant genes and virulence factors were identified by PCR.Homology analysis was performed by multilocus sequencing typing.Whole genome sequencing was performed to analyze the genomic characteristics of CRKP without carbapenemase.Results The 131 strains of CRKP showed resistance to common antibiotics,except for polymyxin B(1.6%resistance rate)and tigacycline(8.0%resistance rate).A total of 105(80.2%)CRKP strains carried the Klebsiella pneumoniae carbapenemase(KPC)resistance gene,15(11.4%)strains carried the New Delhi Metallo-β-lactamase(NDM)gene,and 4(3.1%)isolates carried both KPC and NDM genes.Sequence typing(ST)11(74.0%)was the dominant sequence type.High detection rates for mrkD(96.2%),fimH(98.5%),entB(100%),and other virulence genes were reported.One hypervirulent CRKP strain was detected.The seven strains of CRKP that did not produce carbapenemase were shown to carry ESBL or AmpC genes and had anomalies in membrane porins OMPK35 and OMPK36,according to whole genome sequencing.Conclusion In a large-scale tertiary-care general hospital,CRKP mainly carries the KPC gene,has a high drug resistance rate to a variety of antibiotics,and possesses multiple virulence genes.Attention should be paid to CRKP strains with high virulence.

As the most common chromosomal disorder compatible to life, Down syndrome (DS) is caused by an extra copy of chromosome 21. Almost all DS patients have cognitive dysfunction. Therefore, it is important to study the underlying pathogenetic mechanism to elucidate its molecular basis. This article has provided a review for the molecular mechanisms of NRIP1 and DYRK1A genes, which have been closely associated with the cognitive dysfunctions of DS patients. It has also summarized the research progress on the mechanism of DS and development of new therapeutic strategies based on such studies, with an aim to provide insights into the prevention and treatment for the cognitive dysfunctions in DS patients.

【Objective】 To investigate the predictive value of non-invasive parameters in assessing detrusor function in patients with benign prostatic hyperplasia (BPH). 【Methods】 Clinical data of 384 BPH patients to undergo surgery were enrolled and retrospectively analyzed. The patients’ age and medical history time (MHT) were recorded. The free urinary flow rate was measured and maximum flow rate (Qmax) was recorded. Post-void residual (PVR) and voiding volume (VV) were measured with Bladder Scan, and bladder voiding efficiency (BVE) was calculated. Parameters including detrusor pressure (Pdet@Qmax) and Watts factor (WFmax) were collected in invasive urodynamic examination. Patients were grouped as detrusor underactivity (DU) group and non detrusor underactivity (NDU) group according to the results of WFmax, and the factors influencing detrusor function were analyzed with Logistic regression. The optimal cut-off values were confirmed with receiver operating characteristic (ROC) curve. 【Results】 Significant differences were observed in patients’ age, MHT, Qmax, PVR, BVE, Pdet@Qmax between the DU and NDU groups. Logistic regression showed that the overall prediction accuracy was higher when MHT, Qmax and BVE were included. The model prediction formula was Y=6.020-0.451XMHT+0.554XQmax-0.074XBVE. ROC curve showed when age ≥70.5 years and MHT≥ 7.5 years, there was a greater possibility of DU. When Qmax ≥5.7 mL/s and BVE ≥75.5%, the contractile function of detrusor was normal. Model prediction formula Y≥0.72 showed that detrusor contractility was normal. 【Conclusion】 Age, MHT, Qmax and BVE have certain predictive value for assessing detrusor function in BPH patients.

In vitro studies have established the prevalent theory that the mitochondrial kinase PINK1 protects neurodegeneration by removing damaged mitochondria in Parkinson's disease (PD). However, difficulty in detecting endogenous PINK1 protein in rodent brains and cell lines has prevented the rigorous investigation of the in vivo role of PINK1. Here we report that PINK1 kinase form is selectively expressed in the human and monkey brains. CRISPR/Cas9-mediated deficiency of PINK1 causes similar neurodegeneration in the brains of fetal and adult monkeys as well as cultured monkey neurons without affecting mitochondrial protein expression and morphology. Importantly, PINK1 mutations in the primate brain and human cells reduce protein phosphorylation that is important for neuronal function and survival. Our findings suggest that PINK1 kinase activity rather than its mitochondrial function is essential for the neuronal survival in the primate brains and that its kinase dysfunction could be involved in the pathogenesis of PD.