Efficacy and safety of stellate ganglion block with different volumes of ropivacaine to improve sleep quality in patients with insomnia: a comparative study.

OBJECTIVE: The aim of this study was to compare the efficacy and safety of ultrasound-guided stellate ganglion block (SGB) with different volumes of 0.375% ropivacaine on sleep quality in patients with insomnia. PATIENTS AND METHODS: A total of 80 patients who were selected to undergo SGB for the treatment of insomnia were enrolled. The patients were divided into saline control group, and low-volume (4 mL), medium-volume (6 mL), and high-volume (8 mL) ropivacaine injection groups according to the random table method. The treatment included 7 blocks with once every three days. The left and right stellate ganglions are alternately blocked. The onset and maintenance time of Horner syndrome, the degree of carotid artery dilation and blood flow velocity before and 20 minutes after the first block, the occurrence of complications such as drug crossing of the midline of the artery and hoarse throat were recorded, and the improvement of sleep disorders was evaluated with the Pittsburgh Sleep Quality Index Scale. RESULTS: Horner syndrome occurred in 100% of all volumes of ropivacaine block. The ipsilateral internal carotid artery was dilated and was accompanied by increased blood flow. The degree of dilation and increase in blood flow were not affected by the volumes of drug injection. There were no serious complications in any group, but the incidences of hoarseness and dysphagia were higher in the medium- and high-volume groups than those in the low-volume group (all p < 0.05). Compared with the low- and medium-volume groups, the high-volume group had a faster onset of action, longer maintenance time, and the highest chance of the drug crossing the artery (all p < 0.05). Compared to those before the pre-block and in the control groups, insomnia was improved in all volume groups after the block with nonsignificant intergroup differences. CONCLUSIONS: 4 mL of 0.375% ropivacaine for ultrasound-guided SGB is sufficient to improve the sleep quality of insomnia patients, whose overall risk is lower than block with 6 mL or 8 mL of ropivacaine.

Clinicopathologic and prognostic significance of long non-coding RNA myocardial infarction-associated transcript in multiple cancers.

OBJECTIVE: The aim of the meta-analysis was to explore the clinicopathological and prognostic significance of long non-coding RNA (lncRNA) myocardial infarction-associated transcript (MIAT) in various cancers. MATERIALS AND METHODS: We searched multiple databases, including PubMed, China National Knowledge 53 Infrastructure (CNKI), Springer, Web of Science, and Cochrane, for articles on the prognostic value of lncRNA MIAT in various cancers before 25 March 2021. The odds ratio (OR) and 95% confidence interval (CI) were adopted to evaluate the clinicopathological features and outcomes of cancers. The Cancer Genome Atlas dataset was used to identify the differential expression and prognostic significance of lncRNA MIAT. RESULTS: We enrolled 14 publications, including 1,573 cancer patients. Higher lncRNA MIAT expression was significantly related to worse overall survival (OR=3.13, 95% CI: 2.47-3.96, p<0.05), regardless of cancer types, sample size, and follow-up time of the included studies. Additionally, higher lncRNA MIAT expression was associated with larger tumour sizes (OR=1.67, 95% CI: 1.24-2.26, p<0.05), advanced clinical stage (OR=4.79, 95% CI: 3.38-6.79, p<0.05), lymph nodes metastasis (OR=7.33, 95% CI: 4.61-11.67, p<0.05), and distant metastasis (OR=2.62, 95% CI: 1.88-3.66, p<0.05), but not associated with age and gender. We found no publication bias, and sensitivity analysis indicated that the results were reliable. CONCLUSIONS: Higher lncRNA MIAT expression may predict larger tumour sizes, advanced clinical stage, metastasis of cancers, and lower overall survival rate. LncRNA MIAT may serve as a useful clinicopathological and prognostic biomarker for cancers.

Long noncoding RNA LUCAT1 promotes migration and invasion of prostate cancer cells by inhibiting KISS1 expression.

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 LUCAT1 promotes migration and invasion of prostate cancer cells by inhibiting KISS1 expression, by C. Liu, L. Wang, Y.-W. Li, Y.-S. Cui, Y.-Q. Wang, S. Liu, published in Eur Rev Med Pharmacol Sci 2019; 23 (8): 3277-3283-DOI: 10.26355/eurrev_201904_17689-PMID: 31081080" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/17689.

Long noncoding RNA LUCAT1 promotes migration and invasion of prostate cancer cells by inhibiting KISS1 expression.

OBJECTIVE: Recent researches have revealed the role of long noncoding RNAs (lncRNAs) in tumor development. In this study, the potential function of lncRNA LUCAT1 in the progression of prostate cancer was identified. PATIENTS AND METHODS: Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was used to detect LUCAT1 expression in both prostate cancer cells and tissue samples. Moreover, the association between LUCAT1 expression level and overall survival of prostate cancer patients was analyzed. In addition, wound healing assay and transwell assay were conducted to evaluate the regulatory effect of LUCAT1 on prostate cancer cells. Furthermore, the underlying mechanism of LUCAT1 in regulating the development of prostate cancer was explored via qRT-PCR and Western blot. RESULTS: LUCAT1 expression was much higher in prostate cancer samples than controls. Besides, LUCAT1 expression was correlated with the overall survival of prostate cancer patients. Moreover, LUCAT1 overexpression promoted in vitro migration and invasion of prostate cancer cells. In addition, the mRNA and protein expression of KISS1 were downregulated after LUCAT1 overexpression. Furthermore, it was found that the expression level of KISS1 was negatively related to the expression level of LUCAT1 in prostate cancer tissues. CONCLUSIONS: LUCAT1 could enhance migration and invasion of prostate cancer cells by regulating KISS1, which might offer a potential therapeutic target for prostate cancer.

I/D polymorphism of ACE and risk of diabetes-related end-stage renal disease: a systematic review and meta-analysis.

OBJECTIVE: We conducted a meta-analysis on exploring the correlation between I/D polymorphism of ACE and risk of diabetes mellitus-related end-stage renal disease. MATERIALS AND METHODS: Researches on the correlation between I/D polymorphism of ACE and the risk of diabetes-related end-stage renal disease were searched in the three online databases (PubMed, Embase, and Cochrane Library). Citations of related researches were manually examined and enrolled. This study systematically searched relative literature for cohort studies or case-control studies published in the English language until December 1, 2018. Researches containing odds ratio (OR) and 95% confidence interval (CI) calculated based on the correlation between I/D polymorphism of ACE and the risk of diabetes-related end-stage renal disease were enrolled. The included data were weighted by an inverse variance and then analyzed by a fixed or random effects model. Researches met the inclusion criteria were extracted for relevant data and subjected to a heterogeneity test. The effect size was calculated by STATA 12.0 software for meta-analysis. RESULTS: A total of 15 articles including 1199 cases of diabetes-related end-stage renal disease and 2939 cases of controls were enrolled. I/D polymorphism of ACE remarkably increased the risk of diabetes-related end-stage renal disease. In the subgroup analysis by ethnicity, a significant difference in risk of diabetes-related ESRD was only detected in the Asian population with I/D polymorphism of ACE. However, no significant difference in disease risk was found in the Caucasian population. CONCLUSIONS: This meta-analysis suggested that I/D polymorphism of ACE can markedly increase the incidence of diabetes-related end-stage renal disease, especially in Asian populations.

High expression of carbonic anhydrase 12 (CA12) is associated with good prognosis in breast cancer.

The purpose of this research was to explore whether the expression of carbonic anhydrase 12 (CA12) and the prognosis had a significant relationship in breast cancer patients. A total of 262 breast cancer specimens and 75 normal breast tissue specimens were recruited in this study. The expression of CA12 was detected by immunohistochemistry (IHC), and its correlation with the clinicopathological characteristics of breast cancer patients and their prognosis were further analyzed through standard statistical algorithms. The result of immunohistochemical staining showed that CA12 was detected in both normal breast tissue and breast cancer tissue. Compared to normal breast tissue, CA12 was significant higher expressing in cancer tissues (P=0.009). Statistical analysis showed that the high expression of CA12 in breast cancer tissue was related to estrogen receptor expression level (P<0.001). The follow-up of 262 cases of breast cancer patients within 5 years showed that patients with high expression of CA12 had significant better outcome in DFS (P=0.020) and OS (P=0.019) than patients with low expression of CA12. Univariate analysis of DFS showed that lymph node metastasis (P=0.034) and CA12 (P=0.024) are prognostic indicators. Multivariate analysis manifested that the expression of CA12 (P=0.025) and lymph node metastasis (P=0.024) are two independent factors affecting the prognosis of breast cancer. Conclusion: In breast cancer patients, CA12 can be seen as a new prognostic indicator and even a new target for treatment.

Mitochondria-mediated disturbance of fatty acid metabolism in proximal tubule epithelial cells leads to renal interstitial fibrosis.

The article "Mitochondria-mediated disturbance of fatty acid metabolism in proximal tubule epithelial cells leads to renal interstitial fibrosis" by W. Shen, X.-X. Jiang, Y.-W. Li, Q. He, published in Eur Rev Med Pharmacol Sci 2018; 22 (3): 810-819 has been withdrawn.

Mitochondria-mediated disturbance of fatty acid metabolism in proximal tubule epithelial cells leads to renal interstitial fibrosis.

OBJECTIVE: To investigate the role of mitochondria-mediated fatty acid metabolism in proximal tubule cells in renal interstitial fibrosis. MATERIALS AND METHODS: Intraperitoneal injection of folate was performed to induce renal interstitial fibrosis in mice. Polymerase chain reaction (PCR) was used to detect the expression of cytochrome c oxidase subunit IV (COX4IL) and phosphoenolpyruvate carboxykinase 1 (PCK1) in samples. Electron microscope was used to detect the activity of mitochondria. Serum creatinine and urea nitrogen were chosen as evaluation criteria for renal function. Western-blotting was used to detect protein expression of cells. Immunohistochemistry was used to test renal structure and deposition of collagen. RESULTS: In renal interstitial fibrosis, mitochondria mediated the dysfunction and the promotion of tubulointerstitial fatty acid metabolism. Besides, it could also reduce renal interstitial fibrosis and alleviate the fatty acid metabolism of tubulointerstitial fibrosis. CONCLUSIONS: Mitochondrial dysfunction induced fatty acid metabolism is an important factor to promote the progress of renal interstitial fibrosis. Intervention of related targets of fatty acid metabolism is expected to become a new treatment for renal interstitial fibrosis.

Development of a quantitative PCR assay for monitoring Streptococcus agalactiae colonization and tissue tropism in experimentally infected tilapia.

Streptococcus agalactiae has become one of the most important emerging pathogens in the aquaculture industry and has resulted in large economic losses for tilapia farms in China. In this study, three pairs of specific primers were designed and tested for their specificities and sensitivities in quantitative real-time polymerase chain reactions (qPCRs) after optimization of the annealing temperature. The primer pair IGS-s/IGS-a, which targets the 16S-23S rRNA intergenic spacer region, was finally chosen, having a detection limit of 8.6 copies of S. agalactiae DNA in a 20 µL reaction mixture. Bacterial tissue tropism was demonstrated by qPCR in Oreochromis niloticus 5 days post-injection with a virulent S. agalactiae strain. Bacterial loads were detected at the highest level in brain, followed by moderately high levels in kidney, heart, spleen, intestines, and eye. Significantly lower bacterial loads were observed in muscle, gill and liver. In addition, significantly lower bacterial loads were observed in the brain of convalescent O. niloticus 14 days post-injection with several different S. agalactiae strains. The qPCR for the detection of S. agalactiae developed in this study provides a quantitative tool for investigating bacterial tissue tropism in infected fish, as well as for monitoring bacterial colonization in convalescent fish.

Meta-analysis: silymarin and its combination therapy for the treatment of chronic hepatitis B.

Silymarin is used by many patients with chronic hepatitis B, but its efficacy remains unknown. The aim of this investigation was to conduct a meta-analysis to determine the efficacy and safety of silymarin and its combination therapy for the treatment of chronic hepatitis B. We searched Chinese and English reports from January 1966 to December 2011, using 12 databases. Two reviewers independently screened all reports to identify randomized placebo-controlled trials that evaluated silymarin and its combination therapy for the treatment of chronic hepatitis B. Twelve trials satisfied the eligibility criteria for this meta-analysis. Silymarin was equivalent to antiviral drug or protection liver drugs in serum transaminases, viral load and hepatic fibrosis markers. But silymarin combined with antiviral drug or antiviral drug and protection liver drugs significantly reduced the level of serum transaminases, hepatic fibrosis markers and serum TGF-ß1, TNF-α, IL-6 versus antiviral drug or protection liver drugs. Silymarin combined with protection liver drugs significantly reduced the level of serum transaminases, TBIL, hepatic fibrosis markers and was equivalent to protection liver drugs in the normalisation rates of serum transaminases, TBIL, but protection liver drugs significantly increased the improvement rates of hepatic fibrosis markers. Silymarin combined with antiviral drug or antiviral drug and protection liver drugs may have potential therapeutic value. Treatment with silymarin appears to be safe and well tolerated. The data are too limited to exclude a substantial benefit or harm of silymarin and its combination therapy on serum transaminases, and also to support recommending this herbal compound for the treatment of chronic hepatitis B.

Protein tyrosine phosphatase SHP2 regulates TGF-ß1 production in airway epithelia and asthmatic airway remodeling in mice.

BACKGROUND: Transforming growth factor (TGF)-ß1 produced in airway epithelia has been suggested as a contributor to the airway remodeling observed in asthma patients. The protein tyrosine phosphatase SHP2 is a demonstrable modulator of TGF-ß1 production and thus a potential regulator of airway remodeling. OBJECTIVES: To define the signal event by which SHP2 regulates asthmatic responses in airway epithelial cells by using a mouse model of experimental OVA-induced airway remodeling. METHODS: The airways of Shp2(flox/flox) mice were infected with recombinant adenovirus vectors expressing a Cre recombinase-green fluorescence protein (GFP) fusion protein as part of allergen provocation studies using mice sensitized with ovalbumin (OVA) and repeatedly challenged with OVA. Several endpoint pathologies were assessed, including airway hyper-responsiveness (AHR), lung inflammatory score, peribronchial collagen deposition, and α-smooth muscle actin (SMA) hyperplasia. In vitro studies using airway epithelial cells (BEAS-2B) were used to investigate the role of SHP2 in the regulation of pulmonary remodeling events, including the expression of collagen, α-SMA, and TGF-ß1. RESULTS: Chronic OVA challenges in wild-type mice resulted in airway remodeling and lung dysfunction (e.g., increased inflammatory scores, collagen deposition (fibrosis), smooth muscle hyperplasia, and a significant increase in AHR). These endpoint pathology metrics were each significantly attenuated by conditional shp2 gene knockdown in airway epithelia. In vitro studies using BEAS-2B cells also demonstrated that the level of TGF-ß1 production by these cells correlated with the extent of shp2 gene expression. CONCLUSIONS: SHP2 activities in airway epithelial cells appear to modulate TGF-ß1 production and, in turn, regulate allergic airway remodeling following allergen provocation. CLINICAL IMPLICATIONS: Our findings identify SHP2 as a previously underappreciated contributor to the airway remodeling and lung dysfunction associated with allergen challenge. As such, SHP2 represents a potentially novel therapeutic target for the treatment of asthmatics. CAPSULE SUMMARY: Airway epithelial protein tyrosine phosphatase SHP2 appears to modulate TGF-ß1 activities as part of one or more cellular pathways leading to regulating the airway remodeling and lung dysfunction occurring in mouse models of allergic respiratory inflammation.

Clinical, histopathological and ultrastructural characteristics of naevus depigmentosus.

BACKGROUND: Naevus depigmentosus (ND) is a congenital, nonfamilial, well-circumscribed, uniformly hypopigmented macule, the relative size and distribution of which is stable throughout life. The aetiopathogenesis of ND is not yet fully understood, and reports about the clinical and histopathological characteristics of ND are few. OBJECTIVE: To investigate the clinical and histopathological characteristics of ND, and to make it easier to diagnose ND clinically. METHODS: A clinical survey on 38 patients with ND was performed according to the diagnostic criteria proposed by Coupe. Wood's lamp examination was used to distinguish the different appearance of ND and vitiligo. Skin-biopsy specimens were stained with haematoxylin and eosin, silver, antibodies to S-100 protein, tyrosinase-related protein-1 and tyrosinase, then used for ultrastructural study. Melanocytes were also cultured. RESULTS: Leucoderma was present at birth in 13 patients (34.2%), and appeared during the first 3 years of life in 15 patients. The trunk was the most commonly affected site, and the lesions usually had serrated, irregular borders. Under Wood's lamp, lesions had an off-white accentuation without fluorescence. Immunohistochemistry showed that the melanin content of ND lesions was decreased compared with perilesional normal skin, but there was no change in the number of melanocytes. Ultrastructural study showed that some aggregated melanosomes were present in the affected keratinocytes. CONCLUSION: As a result of the above findings, we suggest changes to Coupe's criteria for ND.

Tophaceous gout of the spine: MR imaging features.

AIM: To define the magnetic resonance (MR) imaging features of tophaceous gout of the spine. MATERIALS AND METHODS: We present the MR imaging examinations of 4 patients with spinal tophaceous gout. Spin-echo T1-weighted and fast spin-echo T2-weighted images were obtained for all patients, and 2 patients had gadolinium-enhanced MR imaging studies. Corresponding computed tomography (CT) was performed in one patient. All images were evaluated for the characteristics of the gouty tophi. RESULTS: The gouty tophi were located at the lower thoracic (n=1) and lumbar (n=3) levels. All tophi yielded homogeneous intermediate to low signal on T1-weighted images and variable signal intensity on T2-weighted images, comprising small foci of very low signal intensity on all sequences. Gadolinium-enhanced MR imaging studies revealed homogeneous enhancement or heterogeneous peripheral enhancement. Diffuse stippled calcifications were found in the tophi on CT images. Periarticular tophi with juxtaarticular bony erosions around facet joints occurred in 3 patients. CONCLUSION: Spinal tophaceous gout should be considered in the differential diagnosis when periarticular deposits contain very low signal foci on all MR imaging sequences.