Correlation study between bone metabolic markers, bone mineral density, and sarcopenia.

OBJECTIVE: To investigate the correlation between bone metabolism markers, bone mineral density (BMD), and sarcopenia. METHODS: A total of 331 consecutive patients aged ≥ 60 years who were hospitalized between November 2020 and December 2021 were enrolled. Participants were divided into sarcopenia and non-sarcopenia groups according to the Asian Working Group on Sarcopenia criteria (AWGS, 2019). The clinical data, bone metabolism markers (ß-CTX, N-MID, and TP1NP), and BMD were compared between the two groups. RESULTS: Age, ß-CTX, and N-MID of the sarcopenia group were higher than those of the non-sarcopenia group (P < 0.05), but the BMD T values were lower than those of the non-sarcopenia group (P < 0.05). Binary logistic regression analysis showed that increased femoral neck BMD (FNBMD) was a protective factor for sarcopenia, while increased ß-CTX was a risk factor. Pearson/Spearman correlation analysis showed that the diagnostic indices of sarcopenia were positively correlated with FNBMD and negatively correlated with ß-CTX and N-MID. Multiple linear regression analysis revealed that BMI and FNBMD significantly positively affected muscle strength and appendicular skeletal muscle mass (ASM). The FNBMD significantly positively affected physical performance, while ß-CTX significantly negatively affected muscle strength, ASM, and physical performance. CONCLUSION: Increased FNBMD may be a protective factor against sarcopenia, and increased ß-CTX may be a risk factor. The FNBMD significantly positively affected the diagnostic indices of sarcopenia, while ß-CTX significantly negatively affected them. BMD and bone metabolism marker levels may be considered in early screening for sarcopenia.

MiR-1269a acts as an onco-miRNA in non-small cell lung cancer via down-regulating SOX6.

The article "MiR-1269a acts as an onco-miRNA in non-small cell lung cancer via down-regulating SOX6, by R.-H. Jin, D.-J. Yu, M. Zhong, published in Eur Rev Med Pharmacol Sci 2018; 22 (15): 4888-4897- DOI: 10.26355/eurrev_201808_15625-PMID: 30070324" has been withdrawn from the authors to some technical reasons (there are some errors and incorrect data). The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/15625.

Long non-coding RNA OR3A4 is associated with poor prognosis of human non-small cell lung cancer and regulates cell proliferation via up-regulating SOX4.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Long non-coding RNA OR3A4 is associated with poor prognosis of human non-small cell lung cancer and regulates cell proliferation via up-regulating SOX4, by M. Zhong, W.-L. Wang, D.-J. Yu, published in Eur Rev Med Pharmacol Sci 2019; 23 (15): 6524-6530-DOI: 10.26355/eurrev_201908_18537-PMID: 31378892" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/18537.

Long noncoding RNA CASC15 is upregulated in non-small cell lung cancer and facilitates cell proliferation and metastasis via targeting miR-130b-3p.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Long noncoding RNA CASC15 is upregulated in non-small cell lung cancer and facilitates cell proliferation and metastasis via targeting miR-130b-3p, by D.-J. Yu, M. Zhong, W.-L. Wang, published in Eur Rev Med Pharmacol Sci 2019; 23 (18): 7943-7949-DOI: 10.26355/eurrev_201909_19010-PMID: 31599419" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/18857.

Correlations of UGT1A1 gene polymorphisms with onset and prognosis of non-small cell lung cancer.

OBJECTIVE: The aim of this study was to investigate the correlations of UDP glucuronosyltransferase family 1 member A1 (UGT1A1) gene polymorphisms with the onset and prognosis of non-small cell lung cancer. PATIENTS AND METHODS: A total of 400 patients with non-small cell lung cancer (disease group) and healthy controls (control group) in our hospital were selected as research subjects. Genomic DNA was extracted from the peripheral blood. UGT1A1 gene polymorphisms rs8330, rs4148323 and rs35003977 were detected after Polymerase Chain Reaction (PCR) amplification. RT-qPCR was performed to measure the expression level of UGT1A1. The survival of patients was analyzed combined with their prognosis. Moreover, the expression of UGT1A1 gene in lung cancer patients from The Cancer Genome Atlas (TCGA) database was analyzed by bioinformatics, and the prognosis was analyzed. RESULTS: According to the expression level of UGT1A1 gene from TCGA and GTEx databases, UGT1A1 gene was highly expressed in lung cancer tissues but lowly expressed in normal lung tissues, and the difference was statistically significant (p<0.05). Combined with the expression level of UGT1A1 and the prognostic information of lung cancer patients from TCGA database, patients with higher expression level of UGT1A1 gene exhibited significantly better prognosis than those with lower level (p=0.0013), suggesting that UGT1A1 gene is an anti-oncogene. There were statistically differences in allele distribution of UGT1A1 gene polymorphism rs8330 between the disease group and control group (p=0.003), and the frequency of allele G was higher in disease group. Moreover, the distribution of genotypes of UGT1A1 gene polymorphisms rs8330 (p=0.006) and rs4148323 (p=0.003) in the disease group was significantly different from that in the control group, and the frequencies of GG genotype of polymorphisms rs8330 and rs4148323 were higher in the disease group. Statistically significant differences in the distribution of recessive models of UGT1A1 gene polymorphism rs8330 were observed between the disease group and control group (p=0.047), and the disease group exhibited a lower frequency of recessive model GC + CC than control group. There were evident differences in the distribution of haplotype GGT of UGT1A1 gene polymorphisms rs8330, rs4148323 and rs35003977 between the disease group and control group (p=0.004), and the frequencies of haplotype GGT were higher in the disease group than those in the control group. UGT1A1 gene polymorphism rs8330 was remarkably associated with gene expression (p<0.05). Meanwhile, the expression of UGT1A1 gene in patients carrying genotype CC declined notably compared with that in patients carrying genotypes GG and GC (p<0.05). Furthermore, the polymorphism rs8330 had a significant correlation with the survival of patients in disease group (p=0.0001), and patients with genotype CC had the worst prognosis. CONCLUSIONS: UGT1A1 gene polymorphisms are prominently correlated with the onset and prognosis of non-small cell lung cancer.

Diverse polarization angle swings from a repeating fast radio burst source.

Fast radio bursts (FRBs) are millisecond-duration radio transients1,2 of unknown origin. Two possible mechanisms that could generate extremely coherent emission from FRBs invoke neutron star magnetospheres3-5 or relativistic shocks far from the central energy source6-8. Detailed polarization observations may help us to understand the emission mechanism. However, the available FRB polarization data have been perplexing, because they show a host of polarimetric properties, including either a constant polarization angle during each burst for some repeaters9,10 or variable polarization angles in some other apparently one-off events11,12. Here we report observations of 15 bursts from FRB 180301 and find various polarization angle swings in seven of them. The diversity of the polarization angle features of these bursts is consistent with a magnetospheric origin of the radio emission, and disfavours the radiation models invoking relativistic shocks.

Linc00703 suppresses non-small cell lung cancer progression by modulating CyclinD1/CDK4 expression.

OBJECTIVE: The aim of this study was to detect the expression of linc00703 in non-small cell lung cancer (NSCLC), and to explore the biological function and potential molecular mechanism of linc00703 in NSCLC using in vitro experiments. PATIENTS AND METHODS: The carcinoma tissues and para-carcinoma tissues were collected from 32 patients diagnosed with NSCLC, from which the RNA was extracted. The relative expression of linc00703 in NSCLC tissues was detected via quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The NSCLC cells and normal human bronchial epithelial cells were selected, in which the relative expression of linc00703 was determined via qRT-PCR. Next, the linc00703 overexpression plasmids were designed and synthesized, and then transiently transfected into NSCLC cells. After 48 h, the overexpression efficiency was detected. Finally, the changes in cell proliferation, apoptosis, cycle distribution and expressions of downstream molecular markers were determined using cell counting kit-8 (CCK8) assay, colony formation assay, flow cytometry and Western blotting, respectively, after overexpression of linc00703 in NSCLC cells. RESULTS: The results of qRT-PCR revealed that the expression of linc00703 was down-regulated by 5.14 times on average in 29 out of 32 cases of NSCLC tissues, and it was also down-regulated in NSCLC cells. Besides, it was found through CCK-8 assay, colony formation assay and flow cytometry that after overexpression of linc00703 in NSCLC cells, the cell proliferation was inhibited, the apoptosis was enhanced, and the cell cycle was arrested in G1/G0 phase. Furthermore, the results of Western blotting showed that after overexpression of linc00703, the protein expressions of cyclinD1 and cyclin-dependent kinase 4 (CDK4) declined, while those of cyclinE1 and CDK2 did not change. CONCLUSIONS: The expression of linc00703 is down-regulated in NSCLC, and it suppresses the occurrence and development of NSCLC via mediating the expression of cyclinD1/CDK4.

MicroRNA-597 inhibits NSCLC progression through negatively regulating CDK2 expression.

OBJECTIVE: Previous studies have shown that microRNA-597 serves as a tumor suppressor gene. However, the role of microRNA-597 in non-small cell lung cancer (NSCLC) has not been fully elucidated. Therefore, the aim of this study was to investigate the expression of microRNA-597 in NSCLC, and to further explore the possible underlying mechanism. PATIENTS AND METHODS: Real-time quantitative polymerase chain reaction (qPCR) was performed to examine microRNA-597 level in tumor tissues and para-cancerous normal tissues collected from 50 patients with NSCLC. The interplay between microRNA-597 expression and clinical indicators, as well as prognosis of NSCLC patients, was analyzed. Meanwhile, qPCR was used to verify microRNA-59 level in NSCLC cell lines. Subsequently, microRNA-597 overexpression and knockdown models were constructed using lentivirus in NSCLC cell lines (including H1299 and PC-9). The impacts of microRNA-597 on the biological functions of NSCLC cells were evaluated using cell counting kit-8 (CCK-8), colony formation, and 5-Ethynyl-2'-deoxyuridine (EdU) assay, respectively. Finally, luciferase reporter gene assay and recovery experiment were performed to investigate the underlying molecular mechanism. RESULTS: QPCR results indicated that microRNA-597 level in NSCLC tissues was remarkably lower than that of adjacent normal tissues, and the difference was statistically significant (p<0.05). Compared with patients with high expression of microRNA-597, patients with low expression of microRNA-597 exhibited significantly higher incidence of pathological stage and lower overall survival rate (p<0.05). Similarly, compared with NC group, the proliferation ability of NSCLC cells was remarkably weakened in microRNA-597 overexpression group (p<0.05). However, the opposite results were observed in microRNA-597 inhibitor group (p<0.05). CDK2 expression was found remarkably elevated in NSCLC cell lines as well as in tissue samples CDK2 expression. Meanwhile, CDK2 expression was negatively correlated with microRNA-597 expression. Luciferase reporter gene assay demonstrated that overexpression of CDK2 could significantly attenuate the luciferase activity of wild-type microRNA-597 vector without attenuating that of mutant vector CDK2 expression. This further suggested that microRNA-597 could target bind to CDK2. Furthermore, cell recovery experiment revealed that CDK2 could reverse the impact of microRNA-597 on the malignant progression of NSCLC. CONCLUSIONS: MicroRNA-597 expression was significantly down-regulated in NSCLC tissues, as well as cell lines. Meanwhile, microRNA-597 expression was associated with the pathological staging and poor prognosis of patients with NSCLC. In addition, microRNA-597 might suppress the malignant progression of NSCLC through the regulation of CDK2.

Long noncoding RNA CASC15 is upregulated in non-small cell lung cancer and facilitates cell proliferation and metastasis via targeting miR-130b-3p.

OBJECTIVE: Recent researches have discovered a class of long noncoding RNAs (lncRNAs), which are dysregulated in various tumors and linked to carcinogenesis. This study aims to uncover the molecular functions of lncRNA CASC15 in non-small cell lung cancer (NSCLC) tumorigenesis. PATIENTS AND METHODS: Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was performed to detect CASC15 expression in 55 NSCLC samples and four NSCLC cell lines. Besides, the function of CASC15 was detected through proliferation assay, transwell assay, and wound healing assay in NSCLC cells. Furthermore, the interaction between CASC15 and miR-130b-3p in NSCLC was studied by performing dual-luciferase reporter assay. In addition, tumor formation and metastasis assay were performed in vivo. RESULTS: CASC15 expression was remarkably upregulated in NSCLC samples compared with that in adjacent samples. Cell proliferation, invasion, and migration in NSCLC were inhibited via knockdown of CASC15 in vitro. Moreover, RT-qPCR results revealed that miR-130b-3p was upregulated via knockdown of CASC15 in vitro. In addition, miR-130b-3p was a direct target of CASC15 in NSCLC. Tumor formation and metastasis were inhibited after CASC15 was knockdown in vivo. CONCLUSIONS: Our study indicates that CASC15 could promote metastasis and proliferation of NSCLC through sponging miR-130b-3p in vitro and in vivo, which may offer a new therapeutic intervention for NSCLC patients.

Long non-coding RNA OR3A4 is associated with poor prognosis of human non-small cell lung cancer and regulates cell proliferation via up-regulating SOX4.

OBJECTIVE: Recent studies have uncovered that long noncoding RNAs (lncRNAs) play a crucial role in the progression of malignant tumors. Non-small cell lung cancer (NSCLC) is a common type of fatal cancer worldwide. The aim of this study was to identify the specific function of lncRNA OR3A4 in the progression of NSCLC, and to explore the possible underlying mechanism. PATIENTS AND METHODS: LncRNA OR3A4 expression in 52-paired NSCLC tissues and adjacent normal tissues was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation assay and cell apoptosis assay were used to investigate the function of OR3A4 in NSCLC. Furthermore, the underlying mechanism was explored by qRT-PCR and Western blot assay. RESULTS: OR3A4 expression was remarkably upregulated in NSCLC tissues when compared with adjacent normal tissues. The overall survival of NSCLC patients in high OR3A4 expression group was significantly worse than those in low OR3A4 expression group. After the silence of OR3A4, the proliferation of NSCLC cells was significantly inhibited. Besides, the apoptosis of NSCLC cells was remarkably promoted after the silence of OR3A4. Meanwhile, knockdown of OR3A4 significantly down-regulated the mRNA and protein levels of SOX4 in NSCLC cells. Furthermore, the expression of SOX4 was found upregulated in both NSCLC tissues and cells. CONCLUSIONS: These above results suggested that OR3A4 could promote cell proliferation and suppress cell apoptosis in NSCLC through up-regulating SOX4. Our findings demonstrated that OR3A4 might serve as a new therapeutic intervention for NSCLC patients.

LncRNA HAGLROS accelerates the progression of lung carcinoma via sponging microRNA-152.

OBJECTIVE: The aim of this study was to analyze the expression profiling of long non-coding RNA (lncRNA) HAGLROS and microRNA-152 in lung carcinoma (LCa), and to explore their regulatory effects on the malignant progression of LCa. PATIENTS AND METHODS: The expression of HAGLROS in 44 paired LCa tissues and matched adjacent tissues was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The correlation between HAGLROS expression and clinical indexes of LCa patients was analyzed. Furthermore, HAGLROS expression in LCa cell lines was detected as well. The HAGLROS over-expression and knockdown models were established in A549 and SPC-A1 cells by transfection of pcDNA-HAGLROS and anti-HAGLROS, respectively. The biological influences of HAGLROS on LCa cells were evaluated through a series of functional experiments. Furthermore, the potential relationship between HAGLROS and microRNA-152 was analyzed. RESULTS: HAGLROS was highly expressed in LCa tissues compared with adjacent normal tissues. LCa patients with a higher expression of HAGLROS presented significantly worse tumor stage, a higher rate of lymphatic metastasis, and a lower survival. The knockdown of HAGLROS significantly attenuated the proliferative and migratory abilities of LCa cells. Meanwhile, HAGLROS over-expression obtained the opposite results. MicroRNA-152 was negatively correlated with HAGLROS in LCa. Rescue experiments showed that the knockdown of microRNA-152 reversed the regulatory effects of HAGLROS on proliferative and migratory abilities of LCa cells. CONCLUSIONS: HAGLROS expression is correlated with tumor stage and lymphatic metastasis of LCa patients. Furthermore, HAGLROS accelerates proliferation and migration of LCa cells by regulating microRNA-152.

LncRNA FBXL19-AS1 promotes proliferation and metastasis via regulating epithelial-mesenchymal transition in non-small cell lung cancer.

OBJECTIVE: To detect the relative expression of long non-coding ribonucleic acid (lncRNA) F-box and leucine-rich repeat protein 19-antisense RNA 1 (FBXL19-AS1) in tissues and cells of non-small-cell lung cancer (NSCLC), and investigate the mechanism of lncRNA FBXL19-AS1 in promoting NSCLC cell proliferation and metastasis by regulating epithelial-mesenchymal transition (EMT) via in vitro experiments. PATIENTS AND METHODS: The relative expression of lncRNA FBXL19-AS1 in NSCLC tissues and cells was detected via quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The colony formation assay was performed to study the impact of interference with lncRNA FBXL19-AS1 expression on NSCLC cell proliferation. The flow cytometry was applied to determine the influence of si-FBXL19-AS1 on the cycle distribution of NSCLC cells. After the interference with lncRNA FBXL19-AS1 expression, the transwell assay was utilized to measure the changes in the migratory and invasive abilities of NSCLC cells, while the expression changes in EMT-related molecular markers was detected via Western blotting. RESULTS: The results of qRT-PCR showed that the expression of lncRNA FBXL19-AS1 in NSCLC tissues and cells was up-regulated. According to the results of the colony formation assay, the proliferative capacity of NSCLC cells was decreased after the interference with lncRNA FBXL19-AS1 expression. In flow cytometry, it was indicated that the cell cycle was arrested at the G0/G1 phase in the experimental group compared with that in the control group. The transwell assay results showed that the migratory and invasive abilities of NSCLC cells were weakened after the interference with lncRNA FBXL19-AS1 expression. The results of the Western blotting assay revealed that the expressions of EMT-related molecular markers (E-cadherin, N-cadherin, etc.) were changed. CONCLUSIONS: The expression of lncRNA FBXL19-AS1 in NSCLC tissues and cells is up-regulated, and the highly expressed lncRNA FBXL19-AS1 can promote NSCLC cell proliferation and metastasis by regulating the EMT.

MiR-1269a acts as an onco-miRNA in non-small cell lung cancer via down-regulating SOX6.

OBJECTIVE: Lung cancer, especially non-small cell lung cancer (NSCLC), remains one of the leading death-causing malignant tumors worldwide. MicroRNAs (miRNAs) have been identified to participate in the development and progression of NSCLC. However, the role of miR-1269a in NSCLC still needs to be elucidated. The objective of this study was to investigate the function of miR-1269a in NSCLC and its underlying mechanism. PATIENTS AND METHODS: Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) was utilized to measure the expression level of miR-1269a in NSCLC tissues and cell lines. After transfection with miR-1269a mimics or inhibitors, the expression level of miR-1269a in NSCLC was up- or down-regulated. Cell Counting Kit-8 (CCK-8) assay and colony formation assay were used to measure cell proliferation ability. Flow cytometry assay was applied to verify the cell cycle distributions of established cell lines. The potential target of miR-1269a was determined by using dual-luciferase and Western blot assays. RESULTS: miR-1269a was significantly over-expressed in NSCLC tissues than that in adjacent normal tissues. The expression of miR-1269a was also up-regulated in NSCLC-derived cell lines. Up-regulation of miR-1269a improved the abilities of cell proliferation, colony formation, and induced cell cycle transition. Meanwhile, down-regulation of miR-1269a decreased the capacities of cell proliferation, colony formation, and arrested the cell cycle. It was further implicated that SOX6 was verified as a target of miR-1269a in NSCLC and over-expressed SOX6 could rescue the effect of miR-1269a up-regulation. CONCLUSIONS: Our study demonstrated that miR-1299a could function as an onco-miRNA in NSCLC and promote NSCLC growth via down-regulating the expression of SOX6.

[Analysis of effects of discipline cooperation on rescue and treatment of severe mass burn patients involved in August 2nd Kunshan factory aluminum dust explosion accident].

Objective: To analyze effects of cooperation between physicians in department of burn surgery and department of intensive care medicine on rescue and treatment of severe mass burn patients involved in August 2nd Kunshan factory aluminum dust explosion accident. Methods: On August 2nd, 2014, 15 extremely severe burn patients involved in August 2nd Kunshan factory aluminum dust explosion accident were admitted to temporary burn treatment center established in Department of Critical Care Medicine of the Second Affiliated Hospital of Soochow University. The 15 patients were equally divided into 3 groups, with 5 patients in each group. Fifteen surgeons and 30 nurses from department of burn surgery and 15 physicians and 30 nurses from department of intensive care medicine from different hospitals in China were divided into 3 groups, with 5 physicians and 10 nurses from department of burn surgery and 5 physicians and 10 nurses from department of intensive care medicine in each group. Each group of physicians and nurses were responsible for treatment of 5 patients. Treatment of patients was leaded by surgeons from department of burn surgery, who were responsible for wound dealing and operation. Physicians from department of intensive care medicine were responsible for systemic treatment and adjustment of relevant equipment's parameters. Volume of fluid infusion and urine output in shock period, severe systemic complication during period of treatment, using time and kind of antibiotics, death in 1 month after admission, length of hospital stay, and survival of patients were monitored. Results: Volume of fluid infusion of 15 extremely severe burn patients within the first 24 hours post injury was 10 360-17 162 (12 998±1 811) mL, including (1.62±0.23) mL·% total body surface area (TBSA)(-1)·kg(-1) electrolyte and colloid and (2 850±232) mL glucose, with electrolyte and colloid ratio of (1.76±0.23)∶1.00. Volume of urine output within the first 24 hours post injury was (2 384±1 242) mL, with (99±52) mL in each hour. Volume of fluid infusion of 15 extremely severe burn patients within the second 24 hours post injury was 8 720-11 616 (9 406±1 277) mL, including (1.04±0.22) mL·%TBSA(-1)·kg(-1) electrolyte and colloid and (2 910±187) mL glucose, with electrolyte and colloid ratio of (1.53±0.31)∶1.00. Volume of urine output within the second 24 hours post injury of patients was (2 299±1 362) mL , with (108±61) mL in each hour. One patient had pulmonary infection, and 7 patients had fungal infection, and no patient had gut microbiota dysbiosis. Patients were treated with combined 2 kinds of antibiotics for 21-85 (50±16) d. No patient died within 1 month after admission. The length of hospital stay was 53-132 (98±44) d. Ten patients survived finally. Conclusions: After being treated by cooperation between physicians in department of burn surgery and department of intensive care medicine, severe mass burn patients involved in August 2nd Kunshan factory aluminum dust explosion accident had hemodynamic stability and could stably experience shock period, with less complication, shorter length of hospital stay, no death within 1 month after admission, more survived patients, which can provide reference for rescue and treatment of severe mass burn patients.

The effects of recombinant human growth hormone (rHGH) on survival of slender narrow pedicle flap and expressions of vascular endothelial growth factor (VEGF) and classification determinant 34 (CD34).

OBJECTIVE: To explore the effects of recombinant human growth hormone (rHGH) on the survival of the mouse slender narrow pedicle flap and the expressions of vascular endothelial growth factor (VEGF) and classification determinant 34 (CD34). MATERIALS AND METHODS: A total of 20 BALB/c mice were randomly divided into the experimental group (n=10) and control group (n=10). The flaps were transplanted for mice in two groups respectively. 6 h after the operation, the mice in the experimental group were administrated with rHGH via local subcutaneous injection, while the mice in the control group were injected with the same amount of normal saline. The laser Doppler was used to measure the sub-flap blood flow rates before the operation, and 3 days, 7 days and 14 days after the operation, respectively; the flap necrosis and survival areas of mice in two groups were measured respectively, and the survival rate of the flap was calculated 14 days after the operation. Afterwards, the flaps of mice in two groups were exfoliated and the shape and structure of flap tissues were tested by the hematoxylin-eosin (HE) staining. Reverse transcription-polymerase chain reaction (RT-PCR) and Western blot were used to test the levels of mRNA and protein of VEGF and CD34 in the flap tissues. RESULTS: The flaps of mice in the control group mainly exhibited the black or grayish-black and lost the elasticity with the hard texture, while those in the experimental group were ruddy in color with favorable elasticity. The survival rate of flaps of mice in the experimental group was significantly higher than that in the control group (83.61 ± 12.56% vs. 46.25 ± 9.70%) and the necrosis area of flaps of mice in the experimental group was significantly smaller than that in the control group (1.32 ± 0.16 vs. 4.13 ± 0.35, p < 0.05). There were no statistical differences in the blood flow rates of mouse flap both before the operation and three days after the operation between two groups (p > 0.05), while the blood flow rates of mouse flap both 7 days and 3 days after the operation in the experimental group were higher than those in the control group (p > 0.05). Compared with those in the control group, the levels of VEGF and CD34 were significantly increased, but the levels of the inflammatory factors of the interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were significantly decreased (p < 0.05). CONCLUSIONS: rHGH plays an active role in the survival of the flap through promoting the angiogenesis and inhibiting inflammatory reaction.

Adipose-derived stem cells improve neovascularization in ischemic flaps in diabetic mellitus through HIF-1α/VEGF pathway.

OBJECTIVE: To investigate the improvement effect of adipose-derived stem cells on neovascularization in an ischemic flap in diabetes mellitus (DM), and to explore the mechanism of hypoxia-inducible factor 1α (HIF-1α)/vascular endothelial growth factor (VEGF) pathway. MATERIALS AND METHODS: A total of 60 male Sprague-Dawley (SD) rats were divided into control group, model group, and adipose-derived stem cells (ADSCs) group. The survival rate of the flap and the number of new blood vessels were measured. The content of VEGF was determined by enzyme-linked immunosorbent assay (ELISA) kit. Then, the expressions of HIF-1α and VEGF in each group were measured by immunohistochemistry. Reverse transcriptase polymerase chain reaction (RT-PCR) method and Western blotting assay were used to detect the mRNA and protein expression of HIF-1α and VEGF in each group. RESULTS: Compared with control group, the flap survival rate of model group was decreased significantly, and the number of new blood vessels was also decreased significantly. Compared with model group, the flap survival rate of ADSCs group was increased significantly, and the number of new blood vessels was also increased significantly. The results of ELISA showed that compared with control group, the level of VEGF in model group was lower than that in model group, and the level of VEGF in the ADSC group was significantly higher than that in the model group. IHC results showed that both HIF-1α and VEGF proteins were decreased significantly in model group, whereas the expression of HIF-1α and VEGF in the ADSCs group was increased significantly. The results of RT-PCR and the Western blotting showed the mRNA and protein expressions in model group were all decreased, while those in ADSCs group were significantly increased (p < 0.05). CONCLUSIONS: ADSCs can improve the neovascularization of diabetic ischemic skin by regulating the HIF-1α/VEGF pathway.

Influences of cisatracurium besylate and vecuronium bromide on muscle relaxant effects and electromyography of tracheal intubation under general anesthesia.

OBJECTIVE: To observe the influences of atracurium besylate and vecuronium bromide on muscle relaxant effects and electromyography of patients with tracheal intubation under general anesthesia in thyroid surgery. PATIENTS AND METHODS: 120 patients treated with thyroid surgery were randomly divided into group A and group V. Patients in group A were administered with cisatracurium besylate combined with propofol and fentanyl for induction of tracheal intubation under general anesthesia. Patients in group V were administered with 0.10 mg/kg vecuronium bromide combined with propofol and fentanyl for induction of tracheal intubation under general anesthesia. Then, the amplitude in electromyography was observed 30-70 min after I.V. muscle relaxant medicine to record the time for patients to reach 0% TW convulsion in abductor pollicis muscle and to observe the muscle relaxant effects. RESULTS: There was no statistical difference in the time to reach 0% TW in two groups (p>0.05). After 30 min of injection of muscle relaxants, EMG positive rate and TW value in group A were significantly higher than those in group V (p<0.05). After 50-70 min of injection of muscle relaxants, EMG positive rate of patients in two groups was up to 100%, and EMG amplitude in group A was significantly higher than that in group V (p<0.05). The time of taking muscle relaxant effects in group A was significantly faster than that in group V (p<0.05), while the recovery time of autonomous respiration and the time of autonomous body activity in group A were slightly lower than those in group V (p>0.05). There was no statistical difference in the time of eye-opening of both groups (p>0.05). MAP and HR of patients in both groups showed no statistical difference before and after injection (p>0.05). CONCLUSIONS: Average EMG amplitude and the positive rate of effective EMG amplitude of cisatracurium besylate are all higher than those of vecuronium bromide. With faster effects and shorter action time, cisatracurium besylate is more suitable in thyroid surgery IONM (intraoperative neurophysiological monitoring).

Hepatitis B virus subgenotype C2- and B2-associated mutation patterns may be responsible for liver cirrhosis and hepatocellular carcinoma, respectively.

The objective of this study was to examine hepatitis B virus (HBV) subgenotypes and mutations in enhancer II, basal core promoter, and precore regions of HBV in relation to risks of liver cirrhosis (LC) and hepatocellular carcinoma (HCC) in Southeast China. A case-control study was performed, including chronic hepatitis B (CHB; n=125), LC (n=120), and HCC (n=136). HBV was genotyped by multiplex polymerase chain reaction and subgenotyped by restriction fragment length polymorphism. HBV mutations were measured by DNA sequencing. HBV genotype C (68.2%) predominated and genotype B (30.2%) was the second most common. Of these, C2 (67.5%) was the most prevalent subgenotype, and B2 (30.2%) ranked second. Thirteen mutations with a frequency >5% were detected. Seven mutation patterns (C1653T, G1719T, G1730C, T1753C, A1762T, G1764A, and G1799C) were associated with C2, and four patterns (C1810T, A1846T, G1862T, and G1896A) were associated with B2. Six patterns (C1653T, G1730C, T1753C, A1762T, G1764A, and G1799C) were obviously associated with LC, and 10 patterns (C1653T, G1730C, T1753C, A1762T, G1764A, G1799C, C1810T, A1846T, G1862T, and G1896A) were significantly associated with HCC compared with CHB. Four patterns (C1810T, A1846T, G1862T, and G1896A) were significantly associated with HCC compared with LC. Multivariate regression analyses showed that HBV subgenotype C2 and C2-associated mutation patterns (C1653T, T1753C, A1762T, and G1764A) were independent risk factors for LC when CHB was the control, and that B2-associated mutation patterns (C1810T, A1846T, G1862T, and G1896A) were independent risk factors for HCC when LC was the control.

Hepatitis B virus subgenotype C2- and B2-associated mutation patterns may be responsible for liver cirrhosis and hepatocellular carcinoma, respectively

The objective of this study was to examine hepatitis B virus (HBV) subgenotypes and mutations in enhancer II, basal core promoter, and precore regions of HBV in relation to risks of liver cirrhosis (LC) and hepatocellular carcinoma (HCC) in Southeast China. A case-control study was performed, including chronic hepatitis B (CHB; n=125), LC (n=120), and HCC (n=136). HBV was genotyped by multiplex polymerase chain reaction and subgenotyped by restriction fragment length polymorphism. HBV mutations were measured by DNA sequencing. HBV genotype C (68.2%) predominated and genotype B (30.2%) was the second most common. Of these, C2 (67.5%) was the most prevalent subgenotype, and B2 (30.2%) ranked second. Thirteen mutations with a frequency >5% were detected. Seven mutation patterns (C1653T, G1719T, G1730C, T1753C, A1762T, G1764A, and G1799C) were associated with C2, and four patterns (C1810T, A1846T, G1862T, and G1896A) were associated with B2. Six patterns (C1653T, G1730C, T1753C, A1762T, G1764A, and G1799C) were obviously associated with LC, and 10 patterns (C1653T, G1730C, T1753C, A1762T, G1764A, G1799C, C1810T, A1846T, G1862T, and G1896A) were significantly associated with HCC compared with CHB. Four patterns (C1810T, A1846T, G1862T, and G1896A) were significantly associated with HCC compared with LC. Multivariate regression analyses showed that HBV subgenotype C2 and C2-associated mutation patterns (C1653T, T1753C, A1762T, and G1764A) were independent risk factors for LC when CHB was the control, and that B2-associated mutation patterns (C1810T, A1846T, G1862T, and G1896A) were independent risk factors for HCC when LC was the control.