BackgroundRumination can play a certain degree role of psychological adjustment in cancer patients. Previous studies have focused on studying the level of rumination in a single type of cancer patient， but there is a lack of comprehensive investigation and influencing factor research on rumination levels in different types of cancer patients. ObjectiveTo explore the level of rumination and its influencing factors among middle-advanced cancer inpatients， so as to provide certain guidance for targeted psychological care in clinical practice. MethodsFrom January 2021 to December 2022， a systematic sampling technique was used to recruit 346 patients with TNM stage III or above tumors hospitalized in Nuclear Industry 416 Hospital， Chengdu Sixth People's Hospital and the First People's Hospital of Yibin. All individuals were assessed using Perceived Social Support Scale （PSSS） and the Chinese version of Event-Related Ruminant Inventory （C-ERRI）， and Logistic regression analysis was utilized to identify the influencing factors of rumination. ResultsIn terms of C-ERRI， patients scored （15.59±5.61） on intrusive rumination and （14.59±5.43） on deliberate rumination. Education levels of junior high school/high school/vocational training school （OR=0.817， P<0.01） and junior college and above （OR=0.579， P<0.05） were the protective factors of intrusive rumination， whereas annual personal incomes of <10 000 yuan （OR=4.918， P<0.01） or 10 000~50 000 yuan （OR=2.076， P<0.01） and low （OR=6.882， P<0.01） or middle （OR=3.114， P<0.01） level of social support were the risk factors of intrusive rumination. For deliberate rumination， education levels of junior high school/high school/vocational training school （OR=0.574， P<0.01） and junior college and above （OR=0.449， P<0.05） were the protective factors， and low （OR=1.391， P<0.01） or middle （OR=1.161， P<0.05） levels of social support were the risk factors. ConclusionThe level of intrusive rumination of inpatients with middle-advanced cancer is related to education level， economic status and social support， furthermore， the level of deliberate rumination is related to the educational level and social support. ［Funded by Medical Research Project of Chengdu Health Commission （ number， 2020119）］

Objective To study the effect of microRNA-183(miR-183)on the growth and development of ze-brafish inner ear,and its mechanism in the regeneration and growth of inner ear hair cells,otocyst and otolith in-jured by cisplatin.Methods Synthesized miRNAs(agomir)and antisense morpholino oligonucleotides(MOs)were injected into zebrafish embryos by microinjection to construct the model of these miRNAs'levels.The 72-hours post fertilization zebrafish were immersed in 50 μmol/L cisplatin for 24 hours.MiRNA microarray analysis,RT-qPCR and other techniques were used to detect the changes of miR-183 and FOXO1 gene expression.FM1-43FX fluores-cence staining was used to understand the injury and regeneration of inner ear nerve thalamic hair cells.The micro-scope was used to observe the growth and development of otocyst and otoliths.Results ① After the treatment of cisplatin,the inner ear hair cells of zebrafish were damaged and the growth and development of otocyst and otoliths were hindered.After the removal of cisplatin,the inner ear hair cells could be regenerated,and the growth and de-velopment of otocyst and otoliths also recovered gradually.② miR-183 was activated after the removal of cisplatin,which was one of the most differentially expressed members in zebrafish larva miRNA(P＜0.001),and the expres-sion level increased continuously to the peak and then gradually returned to the normal level.③ Compared with the control group,after the removal of cisplatin,the overexpression of miR-183 could promote the recovery of the num-ber of hair cells and the area of otocyst and otoliths,while the recovery was inhibited in the group with low expres-sion of miR-183.④ After the removal of cisplatin,FOXO1 was activated and the expression was up-regulated(P＜0.01).When miR-183 was overexpressed,FOXO1 was inhibited and expression was down-regulated(P＜0.01).Conversely,when miR-183 was low,the expression of FOXO1 increased(P＜0.01).Conclusion The increase of miR-183 expression occurs simultaneously with the regeneration of inner ear hair cells and the recovery of growth and development of the otolith area after cisplatin removal.The overexpression or low expression of miR-183 can promote or inhibit the regeneration of inner ear hair cells and the recovery of growth and development of the otolith area,indicating that there is a positive regulatory relationship between them.The mechanism may be related to the negative regulation of miR-183 on FOXO1.

Epidemiological and animal studies indicate that pre-existing diabetes increases the risk of Parkinson's disease(PD).However,the mechanisms underlying this association remain unclear.In the present study,we found that high glucose(HG)levels in the cerebrospinal fluid(CSF)of diabetic rats might enhance the effect of a subthreshold dose of the neurotoxin 6-hydroxydopamine(6-OHDA)on the development of motor disorders,and the damage to the nigrostriatal dopaminergic neuronal pathway.In vitro,HG promoted the 6-OHDA-induced apoptosis in PC12 cells differentiated to neurons with nerve growth factor(NGF)(NGF-PC12).Metabolomics showed that HG promoted hyperglycolysis in neurons and impaired tricarboxylic acid cycle(TCA cycle)activity,which was closely related to abnormal mito-chondrial fusion,thus resulting in mitochondrial loss.Interestingly,HG-induced upregulation of pyruvate kinase M2(PKM2)combined with 6-OHDA exposure not only mediated glycolysis but also promoted abnormal mitochondrial fusion by upregulating the expression of MFN2 in NGF-PC12 cells.In addition,we found that PKM2 knockdown rescued the abnormal mitochondrial fusion and cell apoptosis induced by HG+6-OHDA.Furthermore,we found that shikonin(SK),an inhibitor of PKM2,restored the mito-chondrial number,promoted TCA cycle activity,reversed hyperglycolysis,enhanced the tolerance of cultured neurons to 6-OHDA,and reduced the risk of PD in diabetic rats.Overall,our results indicate that diabetes promotes hyperglycolysis and abnormal mitochondrial fusion in neurons through the upre-gulation of PKM2,leading to an increase in the vulnerability of dopaminergic neurons to 6-OHDA.Thus,the inhibition of PKM2 and restoration of mitochondrial metabolic homeostasis/pathways may prevent the occurrence and development of diabetic PD.

Objective: To analyze the clinical epidemiological characteristics including composition of pathogens , clinical characteristics, and disease prognosis acute bacterial meningitis (ABM) in Chinese children. Methods: A retrospective analysis was performed on the clinical and laboratory data of 1 610 children <15 years of age with ABM in 33 tertiary hospitals in China from January 2019 to December 2020. Patients were divided into different groups according to age,<28 days group, 28 days to <3 months group, 3 months to <1 year group, 1-<5 years of age group, 5-<15 years of age group; etiology confirmed group and clinically diagnosed group according to etiology diagnosis. Non-numeric variables were analyzed with the Chi-square test or Fisher's exact test, while non-normal distrituction numeric variables were compared with nonparametric test. Results: Among 1 610 children with ABM, 955 were male and 650 were female (5 cases were not provided with gender information), and the age of onset was 1.5 (0.5, 5.5) months. There were 588 cases age from <28 days, 462 cases age from 28 days to <3 months, 302 cases age from 3 months to <1 year of age group, 156 cases in the 1-<5 years of age and 101 cases in the 5-<15 years of age. The detection rates were 38.8% (95/245) and 31.5% (70/222) of Escherichia coli and 27.8% (68/245) and 35.1% (78/222) of Streptococcus agalactiae in infants younger than 28 days of age and 28 days to 3 months of age; the detection rates of Streptococcus pneumonia, Escherichia coli, and Streptococcus agalactiae were 34.3% (61/178), 14.0% (25/178) and 13.5% (24/178) in the 3 months of age to <1 year of age group; the dominant pathogens were Streptococcus pneumoniae and the detection rate were 67.9% (74/109) and 44.4% (16/36) in the 1-<5 years of age and 5-<15 years of age . There were 9.7% (19/195) strains of Escherichia coli producing ultra-broad-spectrum β-lactamases. The positive rates of cerebrospinal fluid (CSF) culture and blood culture were 32.2% (515/1 598) and 25.0% (400/1 598), while 38.2% (126/330)and 25.3% (21/83) in CSF metagenomics next generation sequencing and Streptococcus pneumoniae antigen detection. There were 4.3% (32/790) cases of which CSF white blood cell counts were normal in etiology confirmed group. Among 1 610 children with ABM, main intracranial imaging complications were subdural effusion and (or) empyema in 349 cases (21.7%), hydrocephalus in 233 cases (14.5%), brain abscess in 178 cases (11.1%), and other cerebrovascular diseases, including encephalomalacia, cerebral infarction, and encephalatrophy, in 174 cases (10.8%). Among the 166 cases (10.3%) with unfavorable outcome, 32 cases (2.0%) died among whom 24 cases died before 1 year of age, and 37 cases (2.3%) had recurrence among whom 25 cases had recurrence within 3 weeks. The incidences of subdural effusion and (or) empyema, brain abscess and ependymitis in the etiology confirmed group were significantly higher than those in the clinically diagnosed group (26.2% (207/790) vs. 17.3% (142/820), 13.0% (103/790) vs. 9.1% (75/820), 4.6% (36/790) vs. 2.7% (22/820), χ²=18.71, 6.20, 4.07, all P<0.05), but there was no significant difference in the unfavorable outcomes, mortility, and recurrence between these 2 groups (all P>0.05). Conclusions: The onset age of ABM in children is usually within 1 year of age, especially <3 months. The common pathogens in infants <3 months of age are Escherichia coli and Streptococcus agalactiae, and the dominant pathogen in infant ≥3 months is Streptococcus pneumoniae. Subdural effusion and (or) empyema and hydrocephalus are common complications. ABM should not be excluded even if CSF white blood cell counts is within normal range. Standardized bacteriological examination should be paid more attention to increase the pathogenic detection rate. Non-culture CSF detection methods may facilitate the pathogenic diagnosis.
Adolescent ; Brain Abscess ; Child ; Child, Preschool ; Escherichia coli ; Female ; Humans ; Hydrocephalus ; Infant ; Infant, Newborn ; Male ; Meningitis, Bacterial/epidemiology* ; Retrospective Studies ; Streptococcus agalactiae ; Streptococcus pneumoniae ; Subdural Effusion ; beta-Lactamases

During spermatogenesis, developing germ cells that lack the cellular ultrastructures of filopodia and lamellipodia generally found in migrating cells, such as macrophages and fibroblasts, rely on Sertoli cells to support their transport across the seminiferous epithelium. These include the transport of preleptotene spermatocytes across the blood-testis barrier (BTB), but also the transport of germ cells, in particular developing haploid spermatids, across the seminiferous epithelium, that is to and away from the tubule lumen, depending on the stages of the epithelial cycle. On the other hand, cell junctions at the Sertoli cell-cell and Sertoli-germ cell interface also undergo rapid remodeling, involving disassembly and reassembly of cell junctions, which, in turn, are supported by actin- and microtubule-based cytoskeletal remodeling. Interestingly, the underlying mechanism(s) and the involving biomolecule(s) that regulate or support cytoskeletal remodeling remain largely unknown. Herein, we used an in vitro model of primary Sertoli cell cultures that mimicked the Sertoli BTB in vivo overexpressed with the ribosomal protein S6 (rpS6, the downstream signaling protein of mammalian target of rapamycin complex 1 [mTORC1]) cloned into the mammalian expression vector pCI-neo, namely, quadruple phosphomimetic and constitutively active mutant of rpS6 (pCI-neo/p-rpS6-MT) versus pCI-neo/rpS6-WT (wild-type) and empty vector (pCI-neo/Ctrl) for studies. These findings provide compelling evidence that the mTORC1/rpS6 signal pathway exerted its effects to promote Sertoli cell BTB remodeling. This was mediated through changes in the organization of actin- and microtubule-based cytoskeletons, involving changes in the distribution and/or spatial expression of actin- and microtubule-regulatory proteins.
Actins/metabolism* ; Animals ; Blood-Testis Barrier/metabolism* ; Cells, Cultured ; Male ; Mechanistic Target of Rapamycin Complex 1/metabolism* ; Permeability ; Rats ; Ribosomal Protein S6/metabolism* ; Seminiferous Epithelium/metabolism* ; Sertoli Cells/metabolism* ; Signal Transduction/physiology*

Various types of medical devices used in assisted reproductive technologies (ART) should be detected for their safety by strict biological assays. Mouse embryo assay(MEA)has been recognized as one of the most important and standardized methods with the threshold more than 80% of blastocyst formation rate (BR) after 96 h culture of fertilized eggs. The disadvantage using BR for embryonic quality control has been concerned as it is ubiquitously dependent of embryonic morphology and the detailed data including molecular and genetic information is obviously missing and incomplete. This leads to the urgent requirement for more sensitive and efficient assessments for the quality control of ART. This study evaluated the reliability of an immunofluorescent MEA by counting total cell and differential number of the cells in the inner cell mass (ICM) and trophectoderm (TE) in the blastocyst. This method improved the traditional MEA, provided a sensitive and powerful platform to assess embryonic developmental viability and should be suggested as a standard assay to be globally used for the quality control of medical devices and pre-clinical procedures in ART.
Animals ; Blastocyst ; Embryonic Development ; Equipment Safety ; Mice ; Reproducibility of Results ; Reproductive Techniques, Assisted ; instrumentation

Objective To systematically evaluate risk factors for healthcare-associated infection(HAI)with multi-drug-resistant Acinetobacterbaumannii (MDRAB),so as to provide scientific basis for formulating MDRAB pre-vention and intervention strategies. Methods Literatures at home and abroad were searched,RevMan 5.3 statisti-cal software was used for meta analysis of the included literature data. Results A total of 21 papers were included, 8 in English and 13 in Chinese,35 risk factors were analyzed,20 of which were significantly different(all P<0.05),which included in 4 categories:① Related factors for antimicrobial use:use of antimicrobial agents prior to isolation of MDRAB(OR,12.87 [95% CI,5.14-32.21]),duration of antimicrobial use(MD,6.99 [95% CI, 2.21-11.78]),types of used antimicrobial agents (MD,1.07 [95% CI,0.60-1.54]),combined use of antimi-crobial agents(OR,4.16 [95% CI,2.63-6.57]),carbapenems use(OR,3.95 [95% CI,2.54-6.13]),use of third and above generation cephalosporins(OR,2.48 [95% CI,1.90-3.24]);② Related factors for invasive pro-cedures:mechanical ventilation(OR,4.30 [95% CI,3.03- 6.10]),endotracheal intubation/tracheotomy(OR, 4.17 [95% CI,2.41-7.22]),urinary catheterization(OR,2.35 [95% CI,1.42-3.88]),deep venous puncture (OR,2.18 [95% CI,1.14-4.16]),drainage catheterization(OR,2.06 [95% CI,1.19-3.58]);③Related fac-tors for intensive care unit (ICU):ICU admission(OR,5.60 [95% CI,2.73-11.48]),length of ICU stay(MD, 4.21 [95% CI,0.72-7.71]);④ Other factors:heart disease(OR,0.71 [95% CI,0.55-0.93]),tumor(OR, 0.67 [95% CI,0.48-0.95]),pancreatitis(OR,2.04 [95% CI,1.11-3.76]),mixed infection(OR,2.57 [95%CI,1.78-3.71]),length of hospital stay(MD,5.92 [95% CI,3.61-8.23]),APACHE II score(MD,4.56 [95% CI,1.94-7.18]),use of glucocorticoid(OR,2.18 [95% CI,1.21-3.90]). Conclusion Antimicrobial use,invasive operation,ICU-related factors are the main risk factors for MDRAB HAI,the relevant treatment and nursing intervention strategies should be formulated based on risk factors to prevent and reduce MDRAB infection.

The clinical data of 7 patients with porokeratosis (PK) were analyzed retrospectively.In 7 PK patients, 4 cases were disseminated superficial actinic porokeratosis (DSAP),1 case was disseminated superficial porokeratosis (DSP),1 case was giant porokeratosis (GP) and 1 case was hypertrophic porokeratosis (HP).The characteristic cutaneous manifestations were annular well-circumscribed keratotic plaques with slightly atrophic center and elevated border.All patients shared a common histological hallmark, the cornoid lamella.Four cases of DSAP patients had family medical history, consistent with autosomal dominant inheritance.DSP, GP and HP patients denied family medical history.Diagnosis of PK should be based on clinical manifestations, family medical history and histopathological examination.

BACKGROUNDWe showed in our previous study that the N-terminal 17-mer peptide of amyloid precursor protein (APP17-mer peptide), an active peptide segment with trophic and antioxidative effects, protects skin fibroblasts against ultraviolet (UV) damage and downregulates matrix metalloproteinase 1 (MMP-1) expression. The aim of the current study was to explore the protective effects of P165, the N-terminal 5-mer peptide analog of amyloid precursor protein that is resistant to enzymolysis, on UVA-induced damage in human dermal fibroblasts (HDFs).

METHODSHDFs were cultured in Dulbecco's modified Eagle's medium without and with P165 (concentrations were 1, 10, and 100 µmol/L). Then, 15 J/cm(2) UVA irradiation was used to obtain the UV-irradiated model. Cell proliferation was analyzed using MTT kit. The collagen type I and MMP-1 contents in cell lysate were determined by enzyme-linked immunosorbent assay (ELISA). Fluorometric assays were performed to detect the formation of intracellular reactive oxygen species (ROS) in the cells.

RESULTSP165 significantly protected the HDFs against UVA-induced cytotoxicity. Compared with the UVA-irradiated control, 1, 10, and 100 µmol/L P165 elevated cell proliferation by 14.98% (P < 0.05), 17.52% (P < 0.01) and 28.34% (P < 0.001), respectively. Simultaneously, 10 and 100 µmol/L P165 increased collagen type I content (both P < 0.05). Moreover, P165 treatment (all concentrations) also markedly suppressed the UVA-induced MMP-1 expression (all P < 0.001). P165 at 1, 10, and 100 µmol/L also reduced UVA-induced ROS generation by 11.27%, 13.69% (both P < 0.05), and 25.48% (P < 0.001), respectively.

CONCLUSIONSP165 could protect the HDFs against UVA-induced photodamage, including cytotoxicity, and MMP-1 generation. Furthermore, it also increased the collagen type I content in the cells. The inhibitory effect on intracellular ROS generation might be involved in these photoprotective effects. Thus, P165 may be a useful candidate in the prevention and treatment of skin photoaging.

Amyloid beta-Protein Precursor ; pharmacology ; Cells, Cultured ; Fibroblasts ; drug effects ; radiation effects ; Humans ; Skin ; cytology ; Ultraviolet Rays

Abnormalities, Multiple ; epidemiology ; Adolescent ; Child ; Child, Preschool ; Heart Defects, Congenital ; complications ; Humans ; Infant ; Infant, Newborn