Objective:To explore the role of LncRNA NKILA/NF-κB signal pathway in the injury of keratinocytes in oral lichen planus(OLP).Methods:Immortalized human epidermal cells(HaCaTs)were induced by bacterial lipopolysaccharide(LPS)to establish an in vitro cell model of OLP.HaCaTs stably overexpressing NKILA were constructed by lentivirus method.HaCaTs were divided into 4 groups:Control group,Control+LPS group,empty vector infected with lentivirus(NC)+LPS group,overexpressed NKILA(OE)+LPS group.Cell proliferation,apoptosis,total superoxide dismutase(SOD)activity,lipid malondialdehyde oxide(MDA),reactive oxygen species(ROS),expression of related inflammatory factors,p65(nuclear,mass)and NF-κB signaling pathway related protein expression and p65 expression and localization were respectively detected.Results:Compared with Control group,the expression of NKILA,cell proliferation activity and SOD enzyme activity in Control+LPS group were significantly de-creased,while the apoptosis rate,MDA,ROS,IL-6,IL-1β,TNF-α and p65(nuclear and plasma)expression levels were signifi-cantly up-regulated(P＜0.05).Compared with Control+LPS group,the cell proliferation activity and SOD activity were increased in OE+LPS group,and the expression levels of cell apoptosis,MDA,ROS,IL-6,IL-1β,TNF-α and p65(nuclear and plasma)were significantly decreased(P＜0.05),and the localization of p65 protein in the nucleus was significantly decreased in OE+LPS group.Conclusion:LncRNA NKILA may reduce the damage of keratinocytes in oral lichen planus by inhibiting NF-κB signal pathway.

Background Work-related musculoskeletal disorders (WMSDs), as one of the major occupational health issues worldwide, have shown an increasing positive rate year by year. Due to the unique demands of work, operating room nurses exhibit a higher positive rate of WMSDs compared to other occupational groups, necessitating active attention and intervention. Objective To estimate the prevalence of WMSDs among operating room nurses in tertiary hospitals, explore the characteristics and latent categories of WMSDs, and analyze the influencing factors associated with the occurrence of WMSDs. Method Using a randomized cluster sampling method, operating room nurses from nine tertiary hospitals in Urumqi were selected as study participants between December 2023 and January 2024. Data were collected through a general information questionnaire, an ergonomic questionnaire for operating room nurses, and the Chinese Musculoskeletal Disorders Questionnaire. Latent class analysis was employed to examine the patterns of WMSDs among the nurses, while chi-square test and multinomial logistic regression were utilized to analyze the influencing factors of WMSDs. Result A total of 411 valid questionnaires were collected in this survey. The positive rate of WMSDs among operating room nurses in the tertiary hospitals of Urumqi over the past year was 91.9%. The positive rates, ordered from highest to lowest by body region, were neck (79.1%), shoulders (70.3%), and lower back (68.1%). The operating room nurses were categorized into three distinct groups by latent class analysis: multi-site pain group, neck-shoulder-back pain group, and neck and lower back pain group. The results of the multinomial logistic regression models revealed that gender, job strain level, ergonomic load level in the operating room, and exposure to cold or drafty working conditions or not were significant influencing factors for reporting WMSDs among operating room nurses. Specifically, having less than 5 years of work experience, low ergonomic load level, low job strain, and moderate job strain were identified as protective factors against WMSDs. Conversely, exposure to cold or drafty working environments and being female were identified as risk factors for WMSDs. The logistic regression models also indicated that compared to the neck-lower back pain group, the neck-shoulder-back pain group had a higher probability of reporting low job strain (OR=0.168, 95%CI: 0.029, 0.968) and being female (OR=4.847, 95%CI: 2.506, 9.378). In contrast, when comparing to the neck-lower back pain group, the multi-site pain group had a higher probability of reporting, low-level ergonomic workload (OR=0.079, 95%CI: 0.015, 0.412), low job strain (OR=0.019, 95%CI: 0.002, 0.145), moderate job strain (OR=0.080, 95%CI: 0.016, 0.401), high job strain (OR=0.132, 95%CI: 0.027, 0.647), less than 5 years of work experience (OR=0.173, 95%CI: 0.044, 0.683), being female (OR=2.424, 95%CI: 1.130, 5.200), and exposure to cold or drafty working environments (OR=3.277, 95%CI: 1.657, 6.481). Conclusion The positive rate WMSDs among operating room nurses in tertiary hospitals is notably high in Urumqi, with distinct co-occurrence characteristics observed within the population. To mitigate the risk of WMSDs, it is essential to implement targeted health education and prevention training programs tailored to different patterns of WMSDs. Additionally, improving working conditions, optimizing human resource allocation , and other proactive measures should be undertaken. These efforts will effectively reduce the incidence of WMSDs among operating room nurses and safeguard their occupational health.

Inflammatory bowel disease(IBD)is a chronic and recurrent intestinal disease,and has become a major global health issue.Individuals with IBD face an elevated risk of developing colorectal cancer(CRC),and recent studies have indicated that mitochondrial dysfunction plays a pivotal role in the pathogenesis of both IBD and CRC.This review covers the pathogenesis of IBD and CRC,focusing on mitochondrial dysfunction,and explores pharmacological targets and strategies for addressing both conditions by modulating mitochondrial function.Additionally,recent advancements in the phar-macological modulation of mitochondrial dysfunction for treating IBD and CRC,encompassing mitochondrial damage,release of mitochondrial DNA(mtDNA),and impairment of mitophagy,are thoroughly summarized.The review also provides a systematic overview of natural compounds(such as flavonoids,alkaloids,and diterpenoids),Chinese medicines,and intestinal microbiota,which can alleviate IBD and attenuate the progression of CRC by modulating mitochondrial function.In the future,it will be imperative to develop more practical methodologies for real-time monitoring and accurate detection of mitochondrial function,which will greatly aid scientists in identifying more effective agents for treating IBD and CRC through modulation of mitochondrial function.

HDAC7, a member of class IIa HDACs, plays a pivotal regulatory role in tumor, immune, fibrosis, and angiogenesis, rendering it a potential therapeutic target. Nevertheless, due to the high similarity in the enzyme active sites of class IIa HDACs, inhibitors encounter challenges in discerning differences among them. Furthermore, the substitution of key residue in the active pocket of class IIa HDACs renders them pseudo-enzymes, leading to a limited impact of enzymatic inhibitors on their function. In this study, proteolysis targeting chimera (PROTAC) technology was employed to develop HDAC7 drugs. We developed an exceedingly selective HDAC7 PROTAC degrader B14 which showcased superior inhibitory effects on cell proliferation compared to TMP269 in various diffuse large B cell lymphoma (DLBCL) and acute myeloid leukemia (AML) cells. Subsequent investigations unveiled that B14 disrupts BCL6 forming a transcriptional inhibition complex by degrading HDAC7, thereby exerting proliferative inhibition in DLBCL. Our study broadened the understanding of the non-enzymatic functions of HDAC7 and underscored the importance of HDAC7 in the treatment of hematologic malignancies, particularly in DLBCL and AML.

Inflammatory bowel disease (IBD) is a chronic and recurrent intestinal disease, and has become a major global health issue. Individuals with IBD face an elevated risk of developing colorectal cancer (CRC), and recent studies have indicated that mitochondrial dysfunction plays a pivotal role in the pathogenesis of both IBD and CRC. This review covers the pathogenesis of IBD and CRC, focusing on mitochondrial dysfunction, and explores pharmacological targets and strategies for addressing both conditions by modulating mitochondrial function. Additionally, recent advancements in the pharmacological modulation of mitochondrial dysfunction for treating IBD and CRC, encompassing mitochondrial damage, release of mitochondrial DNA (mtDNA), and impairment of mitophagy, are thoroughly summarized. The review also provides a systematic overview of natural compounds (such as flavonoids, alkaloids, and diterpenoids), Chinese medicines, and intestinal microbiota, which can alleviate IBD and attenuate the progression of CRC by modulating mitochondrial function. In the future, it will be imperative to develop more practical methodologies for real-time monitoring and accurate detection of mitochondrial function, which will greatly aid scientists in identifying more effective agents for treating IBD and CRC through modulation of mitochondrial function.

Objective:To explore the role of LncRNA NKILA/NF-κB signal pathway in the injury of keratinocytes in oral lichen planus(OLP).Methods:Immortalized human epidermal cells(HaCaTs)were induced by bacterial lipopolysaccharide(LPS)to establish an in vitro cell model of OLP.HaCaTs stably overexpressing NKILA were constructed by lentivirus method.HaCaTs were divided into 4 groups:Control group,Control+LPS group,empty vector infected with lentivirus(NC)+LPS group,overexpressed NKILA(OE)+LPS group.Cell proliferation,apoptosis,total superoxide dismutase(SOD)activity,lipid malondialdehyde oxide(MDA),reactive oxygen species(ROS),expression of related inflammatory factors,p65(nuclear,mass)and NF-κB signaling pathway related protein expression and p65 expression and localization were respectively detected.Results:Compared with Control group,the expression of NKILA,cell proliferation activity and SOD enzyme activity in Control+LPS group were significantly de-creased,while the apoptosis rate,MDA,ROS,IL-6,IL-1β,TNF-α and p65(nuclear and plasma)expression levels were signifi-cantly up-regulated(P＜0.05).Compared with Control+LPS group,the cell proliferation activity and SOD activity were increased in OE+LPS group,and the expression levels of cell apoptosis,MDA,ROS,IL-6,IL-1β,TNF-α and p65(nuclear and plasma)were significantly decreased(P＜0.05),and the localization of p65 protein in the nucleus was significantly decreased in OE+LPS group.Conclusion:LncRNA NKILA may reduce the damage of keratinocytes in oral lichen planus by inhibiting NF-κB signal pathway.

This study reports the diagnosis and treatment of a 26-year-old pregnant woman with severe malnutrition combined with acute pyelonephritis causing sepsis,refractory septic shock and multiple organ failure.A female patient,26 years old,was admitted to hospital mainly due to"menelipsis for more than 19 weeks,nausea and vomiting for 20 days,fever with fatigue for 3 days".At the end of 19 weeks of in-trauterine pregnancy,the patient presented with fever accompanied by urinary tract irritation.Laboratory tests showed elevated inflammatory indicators,and ultrasonography showed bilateral pelvicalyceal dila-tion.She was diagnosed with acute pyelonephritis,sepsis,acute kidney injury(AKI)and severe malnu-trition.After a whole-hospital consultation,the patient was treated with meropenem and vancomycin as antimicrobial therapy,and bilateral nephrostomy drainage was performed simultaneously.After that,the patient suffered a sudden decrease in blood pressure,blood oxygen saturation,and rapid heart rate.Sep-tic shock with multiple organ dysfunction was considered,and she was transferred to intensive care unit(ICU)immediately.After the patient was transferred to ICU,emergency tracheal intubation and ventila-tor-assisted ventilation were performed.Rapid fluid resuscitation was administered for the patient.While pulse indicator continuous cardiac output(PICCO)monitoring was performed,norepinephrine,terlipres-sin,and methylene blue were administered to maintain peripheral vascular resistance.Since the patient developed septic cardiomyopathy and cardiogenic shock later,levosimendan and epinephrine were admi-nistered to improve cardiac function.While etiological specimens were delivered,meropenem,teicoplanin and caspofungin were given as initial empiric antimicrobial therapy.Unfortunately,the intrauterine fetal death occurred on the night of admission to ICU.On the 3rd day of ICU admission,a still-born child was delivered vaginally with 1/5 defect of the fetal membrane.On the 6th day of ICU admission,the patient had fever again with elevated inflammatory indicators.After excluding infection in other parts,intrau-terine infection caused by incomplete delivery of fetal membrane was considered.Then emergency uterine curettage was performed and the infection gradually improved.Later the laboratory results showed that the nephrostomy drainage was cultured for Escherichia coli and uterine,cervical and vaginal secretions were cultured for Candida albicans.Due to severe infection and intrauterine incomplete abortion,the patient developed disseminated intravascular coagulation(DIC).Active antimicrobial therapy and blood product supplement were given.However,the patient was critically ill with significant decrease in hemoglobin and platelets combined with multiple organ failure.Thrombotic microangiopathy(TMA)was not excluded yet,so plasma exchange was performed for the patient in order not to delay treatment.The patient under-went bedside continuous renal replacement therapy(CRRT)for AKI.The patient was complicated with acute liver injury,and the liver function gradually returned to normal after liver protection,antimicrobial therapy and other treatments.Due to the application of large doses of vasoactive drugs,the extremities of the patient gradually developed cyanosis and ischemic necrosis.Local dry gangrene of the bilateral toes remained at the time of discharge.In general,the patient suffered from septic shock,cardiogenic shock,combined with DIC and multiple organ dysfunction.After infection source control,antimicrobial therapy,uterine curettage,blood purification treatment,nutritional and metabolic support,the patient was dis-charged with a better health condition.

Objective To investigate the effects of long non-coding RNA(lncRNA)TCRGV on the cell biological behavior and lipid metabolism of colorectal cancer(CRC),along with its potential mechanism.Methods The expression level of lncRNA TCRGV in CRC tissues was analyzed using the GEPIA online database.56 pairs of CRC tissues and paracancer tissues were collected.Normal intes-tinal epithelial cells and CRC cell lines were cultured.The expression level of TCRGV in tissues and cell lines was detected using real-time fluorescence quantitative polymerase chain reaction(RT-qPCR).A lentivirus was used to construct a TCRGV overexpression CRC cell model.The effects of TCRGV overexpression on cell migration and invasion capabilities were examined using the Transwell method.The impact of TCRGV on cellular lipid droplet formation was analyzed through Nile red staining.Triglycerides,total cholesterol,and free cholesterol content detection kits were used to detect the content of lipid metabolites in in CRC cells.The expression of the lipid metabo-lism-related protein stearoyl-coenzyme A desaturase 1(SCD1)was detected using RT-qPCR and Western blot to explore its relation-ship with TCRGV.Results The expression level of TCRGV was significantly downregulated in CRC tissues and cells.Compared with the control group,overexpression of TCRGV significantly inhibited the migration and invasion capabilities of CRC cells,significantly de-creased intracellular lipid droplet accumulation,and significantly reduced the contents of total cholesterol,triglycerides,and free choles-terol.The expression level of SCD1 was significantly higher in CRC tissues than that in paracancer tissues.Overexpression of TCRGV sig-nificantly inhibited the expression of SCD1 at both mRNA and protein levels.Conclusion lncRNA TCRGV is downexpressed in CRC and is a potential anticancer molecule.Overexpression of TCRGV may inhibit the cell migration,invasion and lipid reprogramming of CRC by regulating SCD1.

Background::Gastric cancer (GC), a malignant tumor with poor prognosis, is one of the leading causes of cancer-related deaths worldwide; consequently, identifying novel therapeutic targets is crucial for its corresponding treatment. NUF2, a component of the NDC80 kinetochore complex, promotes cancer progression in multiple malignancies. Therefore, this study aimed to explore the potential of NUF2 as a therapeutic target to inhibit GC progression. Methods::Clinical samples were obtained from patients who underwent radical resection of GC at Lanzhou University Second Hospital from 2016 to 2021. Cell count assays, colony formation assays, and cell-derived xenotransplantation (CDX) models were used to determine the effects of NUF2 on GC progression. Flow cytometry was used to detect the effect of NUF2 or quercetin on cell cycle progression and apoptosis. A live-cell time-lapse imaging assay was performed to determine the effect of NUF2 on the regulation of mitotic progression. Transcriptomics was used to investigate the NUF2-associated molecular mechanisms. Virtual docking and microscale thermophoresis were used to identify NUF2 inhibitors. Finally, CDX, organoid, and patient-derived xenograft (PDX) models were used to examine the efficacy of the NUF2 inhibitor in GC. Results::NUF2 expression was significantly increased in GC and was negatively correlated with prognosis. The deletion of NUF2 suppressed GC progression both in vivo and in vitro. NUF2 significantly regulated the mitogen-activated protein kinase (MAPK) pathway, promoted G2/M phase transition, and inhibited apoptosis in GC cells. Additionally, quercetin was identified as a selective NUF2 inhibitor with low toxicity that significantly suppressed tumor growth in GC cells, organoids, CDX, and PDX models. Conclusions::Collectively, NUF2-mediated G2/M phase transition and apoptosis inhibition promoted GC progression; additionally, NUF2 inhibitors exhibited potent anti-GC activity. This study provides a new strategy for targeting NUF2 to suppress GC progression in clinical settings.

Cognitive dysfunction caused by blast traumatic brain injury (bTBI) is a serious neurological disease with high incidence, serious condition and poor prognosis. bTBI can lead to a series of symptoms such as short-term memory loss, inattention or multi-tasking difficulties. In severe cases, bTBI can develop into Alzheimer′s disease, which has a great impact on patients′ normal work and life. At present, researches on cognitive dysfunction caused by bTBI mainly involve model construction, pathogenesis, pathophysiological changes, diagnosis and treatment, etc., and the molecular mechanism of its occurrence remains to be further studied. Under normal physiological conditions, the release of excitatory and inhibitory neurotransmitters, the release and uptake of Ca 2+, oxidation and antioxidant systems, and the promotion and inhibition of apoptosis are in a dynamic balance. bTBI disturbs the balance, which will lead to the damage of nerve cells at the molecular level, thus resulting in the occurrence of cognitive dysfunction. To this end, the authors summarized the aspects of excitatory toxicity and Ca 2+homeostasis disorder, oxidative stress, inflammation and edema, apoptosis, etc., and reviewed the research progress on the molecular mechanism of cognitive dysfunction caused by bTBI, so as to provide a reference for the treatment and rehabilitation of cognitive dysfunction in patients with bTBI.