[Clinical study of the cytokine panel in the diagnosis of ocular chronic graft-versus-host disease].

Objective: To investigate the association between cytokines and ocular chronic graft-versus-host disease (cGVHD) and identify specific biomarkers for ocular cGVHD to enhance clinical diagnosis, treatment, and evaluation. Methods: A mouse model of cGVHD was established to explore the correlation between cGVHD and serum cytokines. Based on the findings from the animal experiments and literature review, a panel of 16 cytokine combinations was identified. Enzyme-linked immunosorbent assay (ELISA) was used to compare the cytokine concentrations in the serum and tear samples from patients who underwent allogeneic hematopoietic stem cell transplantation from June 2017 to March 2022 at the Medical Center of Hematology, Xinqiao Hospital, Army Medical University. Results: ① Compared with the control group, mice with cGVHD exhibited elevated serum IL-1ß, IL-6, IL-8, IL-17, IFN-γ, CX3CL1, CXCL11, CXCL13, CCL11, and CCL19 concentrations (all P<0.05). ② Analysis of the cytokine profiles of the serum and tear samples revealed that compared with patients without ocular cGVHD, those with ocular cGVHD exhibited increased serum IL-8 [P=0.032, area under the curve (AUC) =0.678]; decreased serum IL-10 (P=0.030, AUC=0.701) ; elevated IL-8, IFN-γ, CXCL9, and CCL17 in tear samples; and lower IL-10 and CCL19 in tear samples (all P<0.05, all AUC>0.7). Moreover, cytokines in tear samples showed correlations with ocular surface parameters related to ocular cGVHD. Conclusions: Tear fluid demonstrates greater specificity and sensitivity as a biomarker for diagnosing ocular cGVHD than serum biomarkers. Among the identified cytokines in tear samples, IL-8, IL-10, IFN-γ, CXCL9, CCL17, and CCL19 serve as diagnostic biomarkers for ocular cGVHD post-transplantation, offering practical reference value for diagnosis.

[Budd-Chiari syndrome with hepatopulmonary syndrome: a case report and literature review].

Objective: To summarize the clinical features and prognosis of Budd-Chiari syndrome with hepatopulmonary syndrome (HPS) in children. Methods: The clinical data of a child who had Budd-Chiari syndrome with HPS treated at the Department of Pediatrics of the First Affiliated Hospital of Zhengzhou University in December 2016 was analyzed retrospectively. Taking "Budd-Chiari syndrome" and "hepatopulmonary syndrome" in Chinese or English as the keywords, literature was searched at CNKI, Wanfang, China Biomedical Literature Database and PubMed up to July 2023. Combined with this case, the clinical characteristics, diagnosis, treatment and prognosis of Budd-Chiari syndrome with HPS in children under the age of 18 were summarized. Results: A 13-year-old boy, presented with cyanosis and chest tightness after activities for 6 months, and yellow staining of the skin for 1 week. Physical examination at admission not only found mild yellow staining of the skin and sclera, but also found cyanosis of the lips, periocular skin, and extremities. Laboratory examination showed abnormal liver function with total bilirubin 53 µmol/L, direct bilirubin 14 µmol/L, and indirect bilirubin 39 µmol/L, and abnormal blood gas analysis with the partial pressure of oxygen of 54 mmHg (1 mmHg=0.133 kPa), the partial pressure of carbon dioxide of 31 mmHg, and the alveolar-arterial oxygen gradient of 57 mmHg. Hepatic vein-type Budd-Chiari syndrome, cirrhosis, and portal hypertension were indicated by abdominal CT venography. Contrast-enhanced transthoracic echocardiography (CE-TTE) was positive. After symptomatic and supportive treatment, this patient was discharged and received oxygen therapy outside the hospital. At follow-up until March 2023, there was no significant improvement in hypoxemia, accompanied by limited daily activities. Based on the literature, there were 3 reports in English while none in Chinese, 3 cases were reported. Among a total of 4 children, the chief complaints were dyspnea, cyanosis, or hypoxemia in 3 cases, and unknown in 1 case. There were 2 cases diagnosed with Budd-Chiari syndrome with HPS at the same time due to respiratory symptoms, and 2 cases developed HPS 1.5 years and 8.0 years after the diagnosis of Budd-Chiari syndrome respectively. CE-TTE was positive in 2 cases and pulmonary perfusion imaging was positive in 2 cases. Liver transplantation was performed in 2 cases and their respiratory function recovered well; 1 case received oxygen therapy, with no improvement in hypoxemia; 1 case was waiting for liver transplantation. Conclusions: The onset of Budd-Chiari syndrome with HPS is insidious. The most common clinical manifestations are dyspnea and cyanosis. It can reduce misdiagnosis to confirm intrapulmonary vascular dilatations with CE-TTE at an early stage. Liver transplantation is helpful in improving the prognosis.

[Research progress on exposure to disinfectants and chronic obstructive pulmonary disease].

Chronic obstructive pulmonary disease (COPD) is a common chronic respiratory disease. In recent years, the cumulative prevalence of COPD has been increasing. There are many etiologies and predisposing factors related to COPD, among which occupational risk factors play an important role. Recent studies have found an association between exposure to disinfectants and their products and airway inflammation, respiratory symptoms, and the development of COPD. During the period of COVID-19, disinfection has become an important link in the prevention and control of COVID-19, and the use rate of disinfectants has increased significantly. Therefore, this review summarizes the effects of disinfectants and their products on COPD, discusses the possible mechanisms, and puts forward suggestions for rational use of disinfectants according to the current situation and the development status of disinfectants.

[41 cases of chronic obstructive pulmonary disease caused by occupational irritating chemicals].

Objective: To analyze the case characteristics of Chronic obstructive pulmonary disease caused by occupational irritant chemicals (OI-COPD). To provide basis for revising its diagnostic criteria. Methods: From June to December 2021, we investigated the information of OI-COPD patients confirmed by Shandong Institute of Occupational Health and Prevention of Occupational Diseases, Guangxi Zhuang Autonomous Region Institute of Occupational Disease Prevention and Control, Qingdao Central Hospital affiliated to Qingdao University and other diagnostic institutions in the past five years, a total of 41 cases. The basic information of OI-COPD cases, occupational risk factors exposure information, medical history, smoking history and clinical symptoms were analyzed retrospectively. The measurement data were tested for normal distribution, which was described by x±s, and compared between groups by t test; Those who do not conform to the normal distribution are described by the median [M (Q(1), Q(3)) ] and analyzed by nonparametric test; The counting data were expressed in frequency and rate (% ), and the comparison between groups was tested. Results: Of the 41 cases, 33 were male and 8 were female. The age of the patient diagnosed with OI-COPD was (49.5±10.3) years old, and the minimum age was 30 years old; Among them, 8 patients had a definite long-term smoking history (more than 5 years) ; The exposure duration of occupational risk factors was (18.6±10.3) years, of which 3 patients had exposure duration of less than 5 years; The occupational risk factors leading to OI-COPD include acids and acid-forming compounds, bases, aldehydes, nitrogen oxides, chlorine and its compounds, etc. The exposure level of occupational risk factors is related to the degree of COPD airflow restriction (χ(2)=6.17, P <0.05). 18 patients with diagnosis age <50 years old were diagnosed as early-onset COPD. The incidence of respiratory symptoms in the early diagnosis COPD group was lower than that in the non-early diagnosis COPD group, and the FEV1% pred was significantly higher than that in the non-early diagnosis COPD group. The difference was statistically significant (P<0.01 ) . Conclusion: The exposure level of occupational risk factors may be the risk factor affecting the degree of COPD airflow restriction. With the increase of the exposure level of COPD patients, the proportion of respiratory symptoms will also increase accordingly.

[Knockout of S1PR3 attenuates acute lung injury in mice by inhibiting the MAPK pathway].

OBJECTIVE: To investigate whether knockout of S1PR3 improves lipopolysaccharide (LPS)-induced acute lung injury in mice by inhibiting mitogen activated protein kinases (MAPKs). METHODS: Male C57BL/6J and S1PR3 knockout (S1PR3-/-) mice were both randomized into two groups (n=8) for intratracheal instillation of normal saline or LPS to induce acute lung injury. The expressions of S1PR3, IL-1ß and IL-18 in the lung tissues were detected using RT-qPCR, lung tissue injury was observed with HE staining, and cell apoptosis was detected using flow cytometry. Western blotting was performed to detect the expression levels of caspase-1, GSDMD, p-JNK, p-ERK and p-p38 proteins. In the cell experiment, type II alveolar epithelial cells (MLE-12 cells) were treated with PBS, LPS, CYM5541 (a S1PR3 agonist), or CYM5541 + LPS, and the cell apoptosis and expression levels of MAPK signal pathway molecules were detected. RESULTS: The expression of S1PR3 was up-regulated and serum IL-1ß and IL-18 levels were elevated significantly in the nontransgenic mice with acute lung injury (P < 0.001). By comparison, the elevation of IL-1ß and IL-18 levels was obviously reduced in S1PR3 knockout mice with acute lung injury, which also showed significant improvement of pulmonary hemorrhage, inflammation and exudation, lowered wet-to-dry ratio of the lungs, and decreased cell apoptosis and expressions of cleaved caspase-1 and GSDMD (P < 0.05). In MLE-12 cells, treatment with the S1PR3 agonist significantly increased the expression of pyroptosis-associated proteins (P < 0.05). S1PR3 knockout strongly inhibited the activation of MAPKs family (JNK and ERK p38; P < 0.05), but their expressions were significantly increased following treatment with the S1PR3 agonist (P < 0.05). CONCLUSION: Inhibition of S1PR3 can improve LPSinduced acute lung injury in mice by inhibiting the activation of MAPK signaling.

[Analysis of M2 macrophage infiltration and its clinical significance in 44 patients with multiple primary cancers of the head and neck].

Objective: To investigate and analyze the characteristics of M2 macrophage infiltration and the clinical significance in patients with multiple primary cancers (MPCs) of head and neck in order to explore its role in the diagnosis and prognosis for patients with MPCs. Methods: RNA-seq data were downloaded from the Genomic Data Commons data portal (TCGA) and the R software v4.0.3 was used to statistically analyze the differences. A retrospective analysis was conducted by screening the clinical data of 44 patients (17 males and 27 females) with MPCs in head and neck from July 1998 to February 2016 in the Department of Oral and Maxillofacial Surgery, Peking University School and Hospital of Stomatology. Clinical data from a batch of 41 patients (28 males and 13 females) with gingival cancer and without MPCs from August 2013 to December 2015 were collected and analyzed. The number of CD163 positive cells and the expression patterns in immunohistochemically panoramic slices were observed under high magnification. Chi-square test and Spearman correlation analysis were used to compare the difference and correlation between the CD163 positive counts and/or depths of invasion and the number of incidences. The descriptive statistics on the clinical features was performed by SPSS 25.0. Results: TCGA database analysis showed that the infiltration of macrophage in patients with squamous cell carcinoma of head and neck (HNSCC) was increased compared to the para-cancer sites. A total of 142 tissue samples from 44 patients with MPCs were selected in the present single-center retrospective research. The number of CD163-positive cells in MPCs patients [90.9% (40/44)] was significantly increased compared to single gingival cancer patients [61.0%(25/41)] (r=0.353, P=0.001), which was related to the number of occurrence (r=0.368, P=0.001). The ratio of the CD163 counts in primary tumor to the depths of invasion was positively correlated with the number of onsets (r=0.331, P=0.03). In terms of clinical features, the 44 patients with MPCs were mainly female, non-smoking, no alcohol addiction, no systemic history, Tis-T2 stage and N0 stage squamous cell carcinoma. The number of incidences ranged from two to eight. The incidence of cancer relative to synchronous cancer increased with the increased occurrence of MPCs. The primary cancer mainly occurred in tongue, gingiva and buccal sites, while the proportion of onset sites in gingiva, buccal and palate areas increased with the increased occurrence. Conclusions: M2 type macrophage counts and/or ratio to depth of infiltration were associated with the occurrence of MPCs, which could be used as a clinical indicator to distinguish single and MPCs in HNSCC. For early stage of HNSCC, patients with clinical characters of women, non-smoking, no alcohol addiction, no systemic medical history and sites of tongue, gingiva, and buccal should be paid more attention on their follow-up plan. The findings in the present study was also helpful to explore new treatment methods for the patients with MPCs.

[Treatment efficacy of dietary supplement Licofor for dry eye associated with meibomian gland dysfunction].

Objective: To evaluate the clinical efficacy of dietary supplement Licofor in the treatment of dry eye associated with meibomian gland dysfunction (MGD). Methods: This was a prospective, randomized controlled clinical trial. Sixty patients [25 males, 35 females, aged (42±13) years] who had dry eye associated with MGD were recruited in Xiangya Hospital of Central South University from December 2018 to October 2019. The patients were equally divided into two groups: 30 cases (60 eyes) in the experimental group and 30 cases (60 eyes) in the control group. All subjects were treated with eye hot compress, artificial tears and antibiotic ointment. After that, the experimental group and control group were received dietary supplementary Licofor or placebo daily for 12 weeks. The symptoms and signs of dry eye, morphology and function of meibomian gland, and inflammatory response were assessed at the beginning, 4th, 8th and 12th week of treatment. Results: After 12 weeks of treatment, statistically significant improvements in ocular surface disease index (OSDI) scores, tear break-up time (TBUT), corneal fluorescein staining (CFS), the morphology of eyelid margin, meibomian gland orifice, meibomian gland expressibility, meibum quality, and periglandular inflammatory cell density were determined in both groups (all P<0.05). In the Licofor group, the improvement of OSDI scores [16.7 (12.5, 20.8) vs 20.8 (18.8, 22.9), P<0.001], the morphology of eyelid margin, meibomian gland orifice and periglandular inflammatory cell density [443 (318, 513) vs 553 (415, 676)/mm2, P=0.002] were more significant (all P<0.05). Conclusion: The combined treatment of licofor and conventional treatment can significantly improve symptoms of dry eye, the morphology of eyelid margin, meibomian gland orifice, meibum quality, and eyelid inflammation response of dry eye associated with MGD.

Effects of lncRNA MEG3 on proliferation and apoptosis of gallbladder cancer cells through regulating NF-κB signaling pathway.

OBJECTIVE: To explore the effects of long non-coding ribonucleic acid (lncRNA) maternally expressed gene 3 (MEG3) on proliferation and apoptosis of gallbladder cancer (GBC) cells and its molecular mechanism. MATERIALS AND METHODS: The relative expression level of lncRNA MEG3 in GBC cell lines was detected via quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR). The lncRNA MEG3 expression plasmids were constructed, the cell proliferation ability was detected via Cell Counting Kit-8 (CCK-8) assay and colony formation assay, and the apoptosis was detected via flow cytometry. The effects of lncRNA MEG3 expression on endoplasmic reticulum stress (ERS)-related proteins were determined using Western blotting, and the changes in nuclear factor-κB (NF-κB) protein in the nucleus were determined after overexpression of lncRNA MEG3. RESULTS: The expression of lncRNA MEG3 in three kinds of GBC cell lines was lower than that in human immortalized normal biliary epithelial cells (p<0.05). The results of CCK-8 assay and colony formation assay showed that overexpression of lncRNA MEG3 significantly reduced the proliferation rate and colony formation ability of GBC-SD cells compared with negative control (NC) group (p<0.05, p<0.05). According to the results of flow cytometry, the apoptosis rate was higher in lncRNA MEG63 overexpression group compared with that in NC group (p<0.05). Moreover, the ERS-related proteins (MANF, GRP78, and caspase-3) were remarkably upregulated in lncRNA MEG63 overexpression group compared with those in NC group, indicating that ERS is activated by lncRNA MEG63 overexpression. The NF-κB signal in GBC cells was activated by lncRNA MEG3. CONCLUSIONS: LncRNA MEG3 activates the NF-κB signal in GBC cells to affect the proliferation and apoptosis of GBC cells.

Circ_0000515 drives the progression of hepatocellular carcinoma by regulating MAPK10.

OBJECTIVE: To explore the expression pattern and clinical significance of circ_0000515 in hepatocellular carcinoma (HCC), as well as the molecular mechanism. PATIENTS AND METHODS: Fifty HCC patients were recruited, and their cancer tissues and adjacent normal ones were collected for detecting the differential expression of circ_0000515. The relationship between circ_0000515 and clinical parameters in HCC patients was analyzed. Circ_0000515 knockdown model was generated by lentivirus transfection in Hep3B and MHCC88H cells that were highly expressed with circ_0000515. Regulatory effects of circ_0000515 on phenotypes of Hep3B and MHCC88H cells were examined by Cell Counting Kit-8 (CCK-8) and transwell assay. Target gene of circ_0000515 was verified by Dual-Luciferase reporter assay, and its involvement in HCC progression was detected by rescue experiments. In vivo xenograft model was generated in nude mice aiming to elucidate the role of circ_0000515 in regulating HCC growth. RESULTS: Circ_0000515 was highly expressed in HCC tissues and cell lines. High level of circ_0000515 predicted advanced stage, high incidence of lymphatic metastasis, and low disease-free survival and overall survival in HCC. Knockdown of circ_0000515 attenuated proliferative and migratory abilities in Hep3B and MHCC88H cells. MAPK10, as the target gene binding circ_0000515, was negatively regulated by circ_0000515. Rescue experiments and in vivo xenograft model both indicated that circ_0000515 aggravated the malignant progression of HCC by targeting MAPK10. CONCLUSIONS: Circ_0000515 is upregulated in HCC tissues and cell lines. It can be used for predicting tumor staging, lymphatic metastasis, and prognosis in HCC. Circ_0000515 aggravates the malignant progression of HCC by downregulating MAPK10.

Linc00707 promotes cell proliferation, invasion, and migration via the miR-30c/CTHRC1 regulatory loop in breast cancer.

OBJECTIVE: Breast cancer (BC) is the most common malignant tumor in women. We aimed at investigating the function of long non-coding RNA LINC00707 in BC and the potential mechanism. PATIENTS AND METHODS: The expression level of linc00707 was determined using the quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) in BC tissues and cell lines. The Cell Counting Kit-8 (CCK-8) and colony formation assays were performed to detect the potential influence of LINC0070 on the proliferation ability of the BC cells. Also, the invasion and migration abilities were assessed by the transwell assay. Furthermore, with the bioinformatic analysis and the Dual-Luciferase Reporter Gene Assay, we analyzed the interaction in LINC00707/miR-30c/CTHRC1 regulatory loop. The regulatory effects of LINC00707/miR-30c/CTHRC1 on BC were finally determined. RESULTS: LINC00707 was significantly upregulated in BC tissues and cell lines. The knockdown of LINC00707 inhibited proliferation, invasion, and migration in MDA-MB-231 cells, while the overexpression of LINC00707 achieved the opposite results in MDA-MB-468 cells. LINC00707, acting as a competing endogenous RNA (ceRNA), could sponge miR-30c to upregulate CTHRC1, thus promoting BC progression. CONCLUSIONS: LINC00707 was highly expressed in BC tissues and cells. It promoted cell proliferation, invasion, and migration via miR-30c/CTHRC1 regulatory loop. This might provide a novel target for the diagnosis, treatment, and prognosis for BC.

TGF-ß1 promotes pulmonary arterial hypertension in rats via activating RhoA/ROCK signaling pathway.

OBJECTIVE: To investigate the influence of the Rho/Rho-associated kinase (ROCK) signaling pathway in rats with pulmonary arterial hypertension (PAH) under the intervention with transforming growth factor-beta 1 (TGF-ß1). MATERIALS AND METHODS: A total of 30 rats were divided into three groups using a random number table, including control group (healthy rats, n=10), model group (PAH rats, n=10), and TGF group (PAH rats injected with 5 ng/mL TGF-ß1 recombinant protein, n=10). The systolic blood pressure, ventricular hypertrophy index, pathological changes in lung tissues, TGF-ß1 level, protein, and messenger ribonucleic acid (mRNA) expressions of RhoA and ROCK, as well as concentrations of serum nitric oxide (NO) and endothelin-1 (ET-1) were detected via hemodynamics test, hematoxylin and eosin (HE) staining, immunohistochemical method, reverse transcription-polymerase chain reaction (RT-PCR), and enzyme-linked immunosorbent assay (ELISA). RESULTS: The results of hemodynamics test showed that the right ventricular systolic pressure was increased markedly in model group (46.53±8.81) and TGF group (56.79±9.12) compared with that in control group (26.03±4.21) (p<0.05). The mean pulmonary systolic pressure in model group (25.89±1.92) and TGF group (29.41±1.91) was evidently higher than that in control group (15.77±2.71) (p<0.05). According to the results of heart weight measurement, model group (0.5118±0.1635) exhibited a higher ventricular hypertrophy index than control group (0.2908±0.0313) (p<0.05) but a lower ventricular hypertrophy index than TGF group (0.7231±0.1004) (p<0.05). The medial thickness of the pulmonary artery of the rats was observed through the HE staining. It was found that compared with control group, the medial thickness of the pulmonary artery was increased significantly in model group (p<0.05), while it was raised more prominently in TGF group, higher than that in model group, suggesting that TGF-ß1 expression can increase the medial thickness of the pulmonary artery. It was manifested in immunohistochemical results that the protein expression of RhoA in the left lung tissues rose notably in model group compared with that in control group (p<0.05), and it was also raised remarkably in TGF group in comparison with that in model group (p<0.05), illustrating that the protein expression of TGF can activate the activity of RhoA and ROCK. The results of RT-PCR indicated that the mRNA expressions of RhoA and ROCK in the left lung tissues were elevated distinctly in model group and TGF group compared with those in control group (p<0.05), and the increases were more apparent in TGF group than those in model group (p<0.05). It was revealed in ELISA results that in comparison with control group, model group, and TGF group had markedly increased concentrations of serum NO and ET-1 (p<0.05), while the rises of serum NO and ET-1 concentrations in TGF group were the most prominent compared with those in model group (p<0.05). CONCLUSIONS: Overexpressed TGF-ß1 can activate the RhoA/ROCK signaling pathway, thus promoting the occurrence and development of PAH.

LINC00511 can promote the proliferation, migration and invasion of esophageal cancer cells through regulating microRNA-150-5p.

OBJECTIVE: The aim of this study was to investigate the potential role of LINC00511 in esophageal cancer (ECa), and to explore its underlying mechanism through in vitro cell experiments. PATIENTS AND METHODS: LINC00511 expression in ECa was analyzed by GEPIA database and verified by real-time fluorescence quantitative polymerase chain reaction (qPCR). The bioinformatics website was used to analyze the miRNAs that can bind to LINC00511, and the regulatory relationship between them was verified through Luciferase assay, qPCR as well as Western blotting analysis. Then, the impacts of LINC00511 and microRNA-150-5p on the proliferation or invasiveness of ECa cell lines Kyse30 and ECA109 were investigated by cell counting kit-8 (CCK-8) test and transwell experiment, respectively. Meanwhile, cell cycle and apoptosis were detected by flow cytometry. RESULTS: Analysis results of the GEPIA database revealed that LINC00511 had a significant high expression in ECa tissue samples in comparison with normal control ones, which is consistent with qPCR results. Meanwhile, a significant negative correlation was found between LINC00511 and microRNA-150-5p. In brief, LINC00511 was able to bind to microRNA-150-5p and inhibited its expression. Besides, overexpression of LINC00511 enhanced ECa cell proliferation and migration, accelerated cell cycle, and suppressed cell apoptosis, while transfection with microRNA-150-5p mimics caused the opposite effects. CONCLUSIONS: This study shows for the first time that LINC00511 modulates the progression of ECa by binding to microRNA-150-5p.

[Epidemiological analysis of cytogenetic abnormalities in patients with newly-diagnosed multiple myeloma: a multi-center retrospective study].

Objective: To analyze the frequency and composition of risk-related cytogenetic abnormalities (CAs) in patients with newly-diagnosed multiple myeloma (NDMM) . Methods: The frequency and composition of risk-related CAs from a cohort of 1 015 Chinese patients with NDMM were determined by interphase fluorescence in situ hybridization (iFISH) , individually or in combination. Results: Of the cohort of 1 015 Chinese patients with NDMM, the frequencies of IgH arrangement, del (13q) /13q14, 1q gain and del (17p) were 54.0%, 46.4%, 46.1% (35.8% and 12. 7% for 3 or more than 3 copies) and 9.9%, respectively. Among 454 patients who had the baseline information for all risk-related CAs [except t (14;20) , which was not covered by the FISH panels performed routinely at all five centers], the frequencies of t (4;14) , t (11;14) or t (14;20) were 14.1%, 11.2% and 4.8%, respectively; of them, 44.3% patients carried 2 or more CAs (28.0%, 13.4% and 2.9% for 2, 3 or ≥4 CAs) ; 83.3%, 95.0% or 68.6% patients with 1q gain, del (17p) or IgH rearrangement had 1 or more additional CA (s) , with del (13q) /13q14 as the most frequently accompanied CA; 57.7% patients carried at least 1 HRCA; the incidences of double-hit (DH) MM (DHMM) (=2 HRCAs) and triple-hit (TH) (THMM) (≥3 HRCAs) were 14.3% and 2.9%, respectively. Conclusions: Our results provided an up-to-date profile of CAs in Chinese NDMM patients, which revealed that approximately 58% patients might carry at least 1 HRCA, and 17% could experience so-called DHMM or THMM who presumably had the worst outcome.

Retraction Note to: miR-200 Regulates Epithelial-Mesenchymal Transition in Anaplastic Thyroid Cancer via EGF/EGFR Signaling.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

[Preliminary study of the antibacterial effect on the conjunctival sac and the influence on the corneal epithelium of domestic 5% povidone-iodine before cataract extraction].

Objective: To investigate the efficacy and adverse reactions of 5% povidone-iodine in removing bacteria from the conjunctival sac with different durations. Methods: Randomized controlled study. A total of 420 patients who underwent cataract surgery in Daping Hospital, Army Medical University from December 2017 to June 2018 were selected. Non-surgical eyes (420 eyes) were selected as the study subjects and divided into 4 groups randomly: 30-second group, 1.0-min group, 2.0-min group and 3.5-min group. On the day of surgery, domestic 5% povidone-iodine was used to flush the conjunctival sac for 30 seconds, 1.0 min, 2.0 min and 3.5 min, respectively. The conjunctival sac specimens were collected for bacterial culture and bacterial identification before and after flushing the conjunctival sac with povidone-iodine. The positive rates of bacterial culture and bacterial growth were compared. The patients' ocular surface was observed and the incidence of corneal epithelial injury was recorded at 1 hour and 1 day after surgery. The positive rates of bacterial culture and corneal epithelial injury between groups were compared by Pearson chi-square test. Results: After excluding 20 patients with suspected specimens contamination, 400 patients (400 non-surgical eyes) were enrolled, including 191 males and 209 females, with an average age of 66.8 years. Before flushing the conjunctival sac, the positive rates of bacterial culture in the 30-second group, 1.0-min group, 2.0-min group and 3.5-min group were 44.8% (43/96), 43.3% (39/90), 43.1% (47/109) and 43.8% (46/105), respectively, with no statistically significant difference (χ(2)=0.066, P=0.996). After flushing, the positive rates of conjunctival sac bacterial culture in the 4 groups were 29.2% (28/96), 31.1% (28/90), 13.8% (15/109) and 13.3% (14/105), respectively. The differences between the 30-second group and 2.0-min group (χ(2)=7.308, P=0.007), between the 1.0-min group and 2.0-min group (χ(2)=8.760, P=0.003), between the 30-second group and 3.5-min group (χ(2)=7.606, P=0.006), and between the 1.0-min group and 3.5-min group (χ(2)=9.063, P=0.003) were statistically significant. At 1 hour after surgery, mild corneal epithelial injury occurred in each group, with a rate of 16.7% (16/96), 18.9% (17/90), 20.2% (22/109) and 34.3% (36/105), respectively. The differences between the 30-second group and 3.5-min group (χ(2)=8.118, P=0.004), between the 1.0-min group and 3.5-min group (χ(2)=5.804, P=0.016), and between the 2.0-min group and 3.5-min group (χ(2)=5.383, P=0.020) were statistically significant. At 1 day after surgery, there was no occurrence of new injury, and the incidence of mild corneal injury in each group was 3.1% (3/96), 5.6% (5/90), 9.2% (10/109) and 15.2% (16/105), respectively. There was statistically significant difference between the 30-second group and 3.5-min group (χ(2)=8.597, P=0.003), and between the 1.0-min group and 3.5-min group (χ(2)=4.728, P=0.030). The corneal epithelial injury healed completely at 1 week after surgery. Conclusions: The preoperative bacterial load of the conjunctival sac is more effectively reduced with 5% povidone-iodine in the 2.0-min and 3.5-min than in the 30-second and 1.0-min, and the 2-min is superior to the 3.5-min in the occurrence of corneal epithelial injury at 1 hour after surgery. Irrigation of the conjunctival sac with 5% povidone-iodine for 2 min is effective and safe, which can be an alternative measure. (Chin J Ophthalmol, 2019, 55: 509-514).

[Influences of follow-up methods on rehabilitation and compliance of patients with severe scar after burns].

Objective: To observe the influences of different follow-up methods on rehabilitation and compliance of patients with severe scar after burns. Methods: From January 2012 to May 2016, medical records of 116 patients with severe scar after burns who were admitted to our unit, discharged after wound healing and conforming to the criteria, were retrospectively analyzed. They were divided into face-to-face follow-up group [n=59, 45 males and 14 females, aged (36±9) years] and routine follow-up group [n=57, 44 males and 13 females, aged (35±9) years] based on different follow-up methods they received. On the day of discharge and in post discharge month (PDM) 1, 3, and 6, the Vancouver Scar Scale (VSS) was used to evaluate the hypertrophic scar in joints, Activities of Daily Living (ADL) scale was used to evaluate the disability of patients in the 2 groups. In PDM 1, 3, and 6, Medical Compliance Behavior Questionnaire was used to investigate the medical compliance behaviors of patients in the 2 groups. Data were processed with chi-square test, t test with Bonferroni correction, and analysis of variance for repeated measurement. Results: (1) The VSS score of patients in face-to-face follow-up group on the day of discharge was (11.1±0.7) points, which was close to (11.7±0.7) points of routine follow-up group (t=2.021, P>0.05). The VSS scores of patients in face-to-face follow-up group in PDM 1, 3, and 6 were (10.5±0.6), (8.6±0.7), and (4.7±0.5) points, which were significantly lower than (11.4±0.7), (10.9±1.0), and (9.4±0.8) points of routine follow-up group respectively (t=2.034, 2.033, 2.042, P<0.05 or P<0.01). (2) The ADL score of patients in face-to-face follow-up group on the day of discharge was close to that of routine follow-up group (t=1.781, P>0.05). The ADL scores of patients in face-to-face follow-up group in PDM 1, 3, and 6 were higher than those of routine follow-up group respectively (t=9.683, 8.584, 9.772, P<0.01). (3) The compliance rates of consisted rehabilitation, reasonable diet, and timing consultation of patients in face-to-face follow-up group were better than those of routine follow-up group respectively (χ(2)=19.015, 13.251, 8.652, P<0.01). Conclusions: Compared with routine follow-up by phone, face-to-face follow-up can do better in evaluating the scar condition and ADL of patients with severe scar after burns, and improve the medical compliance rates of patients, which is worthy of clinical promotion.

[Antifibrotic effect of pirfenidone on orbital fibroblasts in patients with thyroid-associated ophthalmopathy and its mechanisms].

Objective: To investigate the effects of pirfenidone on orbital fibroblasts (OFs) from patients with thyroid-associated ophthalmopathy (TAO) and its underlying mechanisms. Methods: OFs from patients with TAO were isolated and cultured in DMEM. Cells were divided into four groups and treated with 0, 250, 500 and 1 000 µg/ml pirfenidone for 24, 48 or 72 hours, respectively. Cell proliferation was detected by tetramethyl azo salt (MTT) assay, and cell viability was determined by trypan blue. Transforming growth factor (TGF) ß1 mRNA level was determined by real-time fluorescence quantitative PCR (RT-qPCR). Type Ⅰ and type Ⅲ collagen secreted from cultured cells were measured by enzyme-linked immuno sorbent assay (ELISA). Results: (1) The primary cultured OFs had typical fibroblast spindle-like morphology. (2) MTT assay showed that pirfenidone treatment significantly inhibited the proliferation of OFs in a dose-dependent manner (P<0.05) with the proliferation rates of pirfenidone treated groups of -15.31%, -24.92%, -48.53% from 250, 500, 1 000 µg/ml after 72 h, respectively, in which the inhibition effect of 1 000 µg/ml pirfenidone was significantly different from the other two treated groups (P<0.05). There were no significant differences in the inhibitory effect of the same concentration group among different time points at 24 h, 48 h and 72 h (P>0.05). Trypan blue showed that the survival rate of OFs in different concentrations of pirfenidone from 0,250, 500, 1 000 µg/ml at 72 h were 78.37%, 79.21%, 78.24% and 76.28%, respectively. There were no significant differences between each drug treated and the control group (P>0.05). (3) RT-qPCR results showed that the mRNA expression levels of TGFß1 at 250, 500, 1 000 µg/ml pirfenidone treated groups at 72 h were 0.760±0.010, 0.440±0.006, and 0.290±0.002, respectively. Compared with the control group (0.950±0.014), the differences were statistically significant (all P<0.05). Moreover, TGFß1 mRNA expression level in 1 000 µg/ml pirfenidone treated group was significantly lower than those in the other two treated groups (all P<0.05). The secretion of type Ⅰ collagen (0.633±0.006, 0.527±0.003 and 0.402±0.008) and type Ⅲ collagen (0.511±0.003, 0.439±0.007 and 0.223±0.006) in 250, 500 and 1 000 µg/ml pirfenidone treated groups at 72 h were significantly lower than those in the control group (0.794±0.005, 0.527±0.007, all P<0.05). Type Ⅰ and type Ⅲ collagen secretion in 1 000 µg/ml pirfenidone treated group were significantly lower than those in the other two groups (P<0.05). Conclusions: Pirfenidone inhibits the cell proliferation, TGFß1 expression and collagen secretion of OFs, which may contribute to the anti-fibrotic effect of pirfenidone.

MiR-874-3p is an independent prognostic factor and functions as an anti-oncomir in esophageal squamous cell carcinoma via targeting STAT3.

OBJECTIVE: Emerging evidence has suggested that dysregulation of miR-874-3p may be involved in tumor development and progression in various types of cancers. However, its expression and biological function in esophageal squamous cell carcinoma (ESCC) remains unclear. The aim of this study was to explore the roles of miR-874-3p in ESCC tumorigenesis and development. PATIENTS AND METHODS: Quantitative Real Time-PCR was used to detect the expression of related mRNAs and miRNA in both ESCC tissues and cells. Then, statistical analysis was performed to determine the associations of miR-874-3p expression with the clinical features and the prognosis of ESCC. Cells proliferation and metastasis were assessed by cell viability assay and transwell assay. Luciferase reporter assays and Western blot were performed to analyze the regulation of putative target of miR-874-3p. RESULTS: We found that the expressions of miR-874-3p in ESCC tissues and cell lines were much lower than that in normal control, respectively. Also, there is a statistically significance between miR-874-3p expression level and lymph nodes metastasis and clinical stage. Kaplan-Meier analysis showed that decreased miR-874-3p expression was associated with poor overall survival of patients. Multivariate Cox regression analysis showed that the expression of miR-874-3p was an independent prognostic factor for ESCC patients. After miR-874-3p mimics transfection, cell proliferation, migration, and invasion were significantly suppressed in the ESCC cells. Mechanistically, STAT3 was confirmed to be the downstream target of miR-874-3p in ESCC cells. CONCLUSIONS: We indicate that miR-874-3p could be a new therapeutic target and prognostic marker of ESCC.