Alexithymia in a Chinese Patient with Chronic Pain and Associated Factors: A Cross-Sectional Study.

BACKGROUND: Alexithymia is more prevalent among those with patients living with chronic pain. Information on the prevalence of alexithymia in Chinese patients with chronic pain and associated factors is limited. AIM: The primary objective of this study was to determine the prevalence of alexithymia, as defined by a score of 61 or greater in the 20-item Toronto Alexithymia Scale (TAS-20), in a Chinese patient with chronic pain. The secondary objective was to investigate the relationship between alexithymia and the clinical and psychological aspects of chronic pain. METHODS: A cross-sectional observational study used the TAS-20 to assess alexithymia of Chinese patients with chronic pain. Sociodemographic and clinical information were obtained and participants filled in the Fear Avoidance Beliefs Questionnaire, Hospital Anxiety and Depression Scale, Pain Catastrophizing Scale, and General Self-efficacy Scale. RESULTS: Of the 346 patients screened, 321 patients living with chronic pain were enrolled into the study. The prevalence of alexithymia among the study population (TAS-20 score ≥61) was 19.6% (95% confidence interval [CI]: 15.3-24.0). The findings showed anxiety (odds ratio [OR] = 2.474; 95% CI, 1.241-4.935), pain catastrophizing (2.649; 1.014-6.921), and self-efficacy (0.952; 0.908-0.988) as independent predictors of alexithymia in patients living with chronic pain. CONCLUSIONS: Patients with chronic pain exhibiting alexithymia were at higher risk of pain catastrophizing, anxiety, and lower self-efficacy, compared with patients without alexithymia. It is important to identify and pay a special attention in clinical practice to patients with chronic pain exhibiting alexithymia, as these individuals are unable to properly express their emotions.

Knowledge, attitude, and practice of nurses in intensive care unit on preventing medical device-related pressure injury: A cross-sectional study in western China.

The knowledge, attitude, and practice of nurses in intensive care units (ICUs) are determinants for the efficacy of preventing the medical device-related pressure injury (MDRPI). The aim of this study was to determine the level and factors of knowledge, attitude, and practice of nurses' ICUs on preventing medical MDRPI in western China. An annual cross-sectional study was conducted in hospitals of western China from May 2020 to September 2020. Nurses' knowledge and attitudes were assessed using Clinical Nurses Prevention MDRPI of Critically Ill Patients for the Knowledge, Attitude, Practice Assessment Scale. SPSS software version 25.0 and independent t-test, Chi-square, Fisher exact, one-way analysis of variance, and multiple linear regression tests were used for data analysis. A total of 1002 nurses in ICUs from 37 hospitals in Gansu Province, China, participated in this study. The scores of overall KAP, knowledge, attitudes, and practice were 149.17 ± 24.62, 53.83 ± 12.23, 37.24 ± 6.35 and 58.10 ± 9.83, respectively. There was a positive and significant relationship between three variables. Findings revealed that nurses' knowledge score in the Tertiary hospital was higher than scores of other hospitals as 3.840 units. Moreover, the knowledge score and practice score of nurses with bachelor's degree or above were higher than other nurses and are 0.978 and 1.106 units, respectively. Based on the findings, practice of nurses increased by 0.992 units, with a 1-year increase in work experience of nurses in the ICU. The levels of knowledge, attitude, and practice of nurse in ICUs on preventing MDRPI were acceptable. The findings of the study highlight that a comprehensive approach should be conducted for raising the level of knowledge, attitude, and practice of nurses' ICUs on preventing medical MDRPI, as well as improving the quality of care for critically ill patients.

The potassium channel KCa3.1 promotes cell proliferation by activating SKP2 and metastasis through the EMT pathway in hepatocellular carcinoma.

The intermediate conductance calcium-activated potassium channel (KCa3.1) plays an important role in maintaining intracellular calcium homeostasis and is involved in the tumorigenesis of many human cancers. However, it is unknown whether KCa3.1 plays a role in the genesis of hepatocellular carcinoma (HCC), one of the most common malignant tumors worldwide with a very poor prognosis. In our study, we found that the expression of KCa3.1 was significantly elevated in poorly differentiated HCC tissues compared to adjacent noncancerous tissues. In vitro and in vivo experiments showed that KCa3.1 could promote cell proliferation, migration, and invasion of HCC. Mechanistically, KCa3.1 promoted cell cycle progression and migration and invasion of HCC cells by activating S-phase protein kinase 2 (SKP2) to trigger the degradation of p21 and p27 and targeting Reelin (RELN) to induce epithelial-mesenchymal transition (EMT), respectively. Taken together, our results demonstrate that KCa3.1 plays an important role in the genesis and progression of HCC, implying that it might be a promising therapeutic target in HCC.

Inhibition of KLHL21 prevents cholangiocarcinoma progression through regulating cell proliferation and motility, arresting cell cycle and reducing Erk activation.

Kelch-like family member 21 (KLHL21) is involved in cell mitosis and motility. Nevertheless, the clinical significance and biological function of KLHL21 in cholangiocarcinoma (CCA) are elusive. This is the first study to describe a pivotal role for KLHL21 in the progression of CCA. The expression of KLHL21 was elevated in CCA tissues compared with paired normal bile duct tissues. In addition, immunohistochemical and statistical analyses demonstrated that the expression of KLHL21 correlated inversely with tumor histological grade (p < 0.05) and the overall survival of patients (p < 0.01). In CCA cells, we found that the inhibition of KLHL21 significantly reduced proliferation, migration and invasion. Further results indicated that inhibition of KLHL21 triggered G0/G1 cell cycle arrest, leading to the increased expression of P21 and P27 and decreased expression of Cyclin E1, which eventually resulted in proliferation suppression in CCA cells. Furthermore, KLHL21 knockdown alleviated the activation of the Erk signaling pathway via decreasing the expression of phospho-Erk1/2. Our data demonstrated that KLHL21 plays an essential role in the tumorigenesis and progression of CCA, implying that it might serve as a potential therapeutic target for CCA treatment.

Management of intrahepatic splenosis:a case report and review of the literature.

BACKGROUND: Splenosis is the heterotopic autotransplantation and implantation of splenic tissue after splenic trauma or splenectomy. Considering that splenosis often occurs in the mesentery, omentum, and peritoneum, intrahepatic splenosis has seldom been reported. We report a rare case of isolated intrahepatic splenosis in a 54-year-old man who presented with a liver mass thought to be hepatocellular carcinoma. CASE PRESENTATION: A 54-year-old man was referred to our hospital for further evaluation of a liver lesion. The patient was asymptomatic and had a history of emergent splenectomy after a high-altitude falling accident. Abdominal contrast-enhanced computed tomography revealed a 4.5 × 3.3 cm lesion that was located in segment IV of the left liver lobe. The lesion had an inhomogeneous enhancement during the arterial phase and diminished enhancement during the portal and equilibrium phases. Similar radiological features were also observed on a contrast magnetic resonance imaging scan. Partial hepatectomy was performed with the suspicion of hepatocellular carcinoma. Pathological examination of the liver specimen revealed intrahepatic splenosis. CONCLUSION: Splenosis should be considered in differential diagnosis of a liver mass discovered years after splenic trauma or surgery. A proposed scoring system may be helpful in evaluating the suspicious degree of intrahepatic mass to be splenosis. Invasive treatments are not recommended for asymptomatic patients, since the splenosis can provide beneficial immunologic function.

Sternomastoid intermuscular approach has better postoperative cosmesis and less neck discomfort than linea alba cervicalis approach in hemithyroidectomy: a randomized clinical trial.

BACKGROUND: Surgery is still the most important treatment method for thyroid cancer. The classic linea alba cervicalis approach caused obvious neck scarring. This study explored an alternative open operative approach with concealed incision for hemithyroidectomy, and demonstrated whether it was non-inferior to traditional approach in postoperative complications and operation efficiency. METHODS: Patients ( n =220) from November 2019 to November 2020 willing to undergo hemithyroidectomy because of differentiated thyroid cancer were randomly divided into the sternocleidomastoid intermuscular approach (SMIA) group ( n =110), and the linea alba cervicalis approach (LACA) group ( n =110). The incidence of postoperative complications within 3 months and operation efficiency indicator R0 resection rate were recorded as primary endpoint, while scar apperance was assessed as secondary endpoint. The data were statistically analyzed. RESULTS: The baseline data of these two groups were comparable, with no significant difference ( P >0.05). As primary endpoint, R0 resection rate was 100% in both groups. In the 1-month follow-up period, the SMIA group had a lower score for neck discomfort compared with that of the LACA group (1.01±0.1648 vs. 0.5657±0.0976, P =0.0217). The SMIA group's scar had better results from the observer scar assessment compared to that of the LACA group as secondary endpoint. Within the 3-month follow-up, the total complications were calculated, and it was demonstrated that SMIA was non-inferior to traditional LACA operation ( P of non-inferiority=0.0048). CONCLUSIONS: Compared with LACA group, surgery through the SMIA is safe, effective, and has non-inferior postoperative complications. SMIA can be considered an alternative approach to classic LACA in hemithyroidectomy.

Targeting anillin inhibits tumorigenesis and tumor growth in hepatocellular carcinoma via impairing cytokinesis fidelity.

Targeting cytokinesis can suppress tumor growth by blocking cell division and promoting apoptosis. We aimed to characterize key cytokinesis regulator in hepatocellular carcinoma (HCC) progression, providing insights into identifying promising HCC therapeutic targets. The unbiased bioinformatic screening identified Anillin actin binding protein (ANLN) as a critical cytokinesis regulator involved in HCC development. Functional assay demonstrated that knockdown of ANLN inhibited HCC growth by inducing cytokinesis failure and DNA damage, leading to multinucleation and mitotic catastrophe. Mechanistically, ANLN acts as a scaffold to strengthen interaction between RACGAP1 and PLK1. ANLN promotes PLK1-mediated RACGAP1 phosphorylation and RhoA activation to ensure cytokinesis fidelity. To explore the function of ANLN in HCC tumorigenesis, we hydrodynamically transfected c-Myc and NRAS plasmids into Anln+/+, Anln+/-, and Anln-/- mice through tail vein injection. Hepatic Anln ablation significantly impaired c-Myc/NRAS-driven hepatocarcinogenesis. Moreover, enhanced hepatic polyploidization was observed in Anln ablation mice, manifesting as increasing proportion of cellular and nuclear polyploidy. Clinically, ANLN is upregulated in human HCC tissues and high level of ANLN is correlated with poor patients' prognosis. Additionally, the proportion of cellular polyploidy decreases during HCC progression and ANLN level is significantly correlated with cellular polyploidy proportion in human HCC samples. In conclusion, ANLN is identified as a key cytokinesis regulator contributing to HCC initiation and progression. Our findings revealed a novel mechanism of ANLN in the regulation of cytokinesis to promote HCC tumorigenesis and growth, suggesting targeting ANLN to inhibit cytokinesis may be a promising therapeutic strategy for HCC.

EAG1 enhances hepatocellular carcinoma proliferation by modulating SKP2 and metastasis through pseudopod formation.

Ether-à-go-go-1 (EAG1), one of the potassium channels, is involved in various physiological processes and plays an important role in the tumorigenesis of many kinds of cancer. EAG1 is highly expressed in hepatocarcinoma cells and is closely related to clinical prognosis, but the molecular mechanism remains elusive. In this study, we verified that EAG1 promotes the proliferation of hepatocellular carcinoma (HCC) both in vitro and in vivo. It promotes cell cycle progression by inhibiting the ubiquitination of SKP2. In addition, EAG1 promotes the migration and invasion of HCC by promoting cell pseudopod formation. Furthermore, in a high-pressure plasmid-injected mouse liver orthotopic carcinoma model, astemizole, an EAG family blocker, can significantly inhibit the formation of liver cancer. Meanwhile, liver-specific EAG1 knockout mice show resistance to hepatocarcinogenesis. This research demonstrated that EAG1 plays an important role in the progression of HCC, and could be a potential therapeutic target for HCC.

Prevalence of suicidal ideation, suicide attempt, and suicide plan among HIV/AIDS: A systematic review and meta-analysis.

BACKGROUND: Suicidality is common in people living with HIV/AIDS. However, the prevalence estimates of the suicidality vary between studies. Here, we performed a systematic review and estimated the prevalence of suicidal behavior in this population. METHODS: Systematic search of PubMed, Embase, Web of Science, CINAHL, Scopus and PsycINFO for relevant studies published before August 29, 2020. A random-effects model was used to pool the estimates of the prevalence of suicidal ideation, attempts and plans, which were also stratified by continent or region and screening instrument from the studies included in this meta-analysis. RESULTS: Suicide prevalence data were extracted from 36 studies(n=32,818) from 15 countries. The overall pooled crude prevalence estimates of suicidal ideation, plans, and attempts were 20.9% [95% confidence interval (CI) 16.5-21.6%],8.1% (95% CI 5.4-11.3%), and 7.5% (95% CI 5.7-9.5%), respectively. For lifetime suicidal ideation and attempts prevalence, this was 22.4% (95% CI 15.9-29.8%), and 12.0% (95% CI 6.9- 18.1%), respectively. Summary prevalence estimates ranged across assessment modalities from 6.5% to 33.7%. Pooled estimates were generally higher for females, as compared with males (risk ratios in the range 1.48-1.85). The leave-one-out analysis showed that no single study significantly affected the final pooled results.

Downregulation of MGMT promotes proliferation of intrahepatic cholangiocarcinoma by regulating p21.

BACKGROUND: Intrahepatic cholangiocarcinoma (ICC) is one of the most devastating cancers of the gastrointestinal tract. It is crucial to determine the accurate prognostic factors and find new therapeutic strategies. Meanwhile, O6-methylguanine-DNA methyltransferase (MGMT) is associated with malignant tumor progression. Thus, further studies are needed to investigate whether MGMT plays a similar role in ICC. MATERIALS AND METHODS: Quantitative real-time PCR, western blot, and immunohistochemistry staining were used to detect the expression of MGMT in ICC tissues. The correlations between MGMT expression and clinicopathologic features were analyzed. The cell-proliferation assay and colony-formation assay were applied to evaluate proliferation ability, while methylation-specific PCR were used to detect the methylation status of the MGMT promoter CpG island in ICC tissues and cells. RESULTS: Our study found that the expression of MGMT was decreased in ICC tissues when compared with paired normal tissues. In addition, we demonstrated that MGMT expression was positively correlated with overall survival rates and tumor histological grade. Silencing of MGMT significantly promoted cell proliferation in ICC. Further research showed that silencing of MGMT induced cells to enter S phase by inhibiting p21, p27, and Cyclin E expression, ultimately promoting ICC proliferation. We also demonstrated that the MGMT promoter was highly methylated in ICC, and the levels of MGMT and p21 mRNA increased after DNA demethylation. In addition, the levels of MGMT and p21 protein were positively correlated in ICC tissues. CONCLUSION: MGMT may play a critical role in carcinogenesis and the development of ICC, and provides a new marker of clinical prognosis and target for ICC treatment.

Regeneration of a Bioengineered Thyroid Using Decellularized Thyroid Matrix.

BACKGROUND: Hypothyroidism is a common hormone deficiency condition. Regenerative medicine approaches, such as a bioengineered thyroid, have been proposed as potential therapeutic alternatives for patients with hypothyroidism. This study demonstrates a novel approach to generate thyroid grafts using decellularized rat thyroid matrix. METHODS: Isolated rat thyroid glands were perfused with 1% sodium dodecyl sulfate to generate a decellularized thyroid scaffold. The rat thyroid scaffold was then recellularized with rat thyroid cell line to reconstruct the thyroid by perfusion seeding technique. As a pilot study, the decellularized rat thyroid scaffold was perfused with human-derived thyrocytes and parathyroid cells. RESULTS: The decellularization process retained the intricate three-dimensional microarchitecture with a perfusable vascular network and native extracellular matrix components, allowing efficient reseeding of the thyroid matrix with the FRTL-5 rat thyroid cell line generating three-dimensional follicular structures in vitro. In addition, the recellularized thyroid showed successful cellular engraftment and thyroid-specific function, including synthesis of thyroglobulin and thyroid peroxidase. Moreover, the decellularized rat thyroid scaffold could further be recellularized with human-derived thyroid cells and parathyroid cells to reconstruct a humanized bioartificial endocrine organ, which maintained expression of critical genes such as thyroglobulin, thyroid peroxidase, and parathyroid hormone. CONCLUSION: These findings demonstrate the utility of a decellularized thyroid extracellular matrix scaffold system for the development of functional, bioengineered thyroid tissue, which could potentially be used to treat hypothyroidism.

KCa3.1 as an Effective Target for Inhibition of Growth and Progression of Intrahepatic Cholangiocarcinoma.

Background: Intrahepatic cholangiocarcinoma (ICC) is a high malignant tumor arising from the bile ducts in the liver with a poor prognosis. As current molecular targeted therapies and systemic chemotherapies had limited success in ICC, novel therapeutic targets are needed. In this study, we attempted to investigate the expression and the role of the intermediate conductance calcium-activated potassium channel (KCa3.1) in ICC. Methods: The expression levels of KCa3.1 channel were measured in 81 resected ICC tumor specimens and the clinicopathological significance of these levels were determined. KCa3.1 channel inhibitor and siRNA were used to study the role of KCa3.1 in proliferation, migration, and invasion of ICC cell lines. The effect of KCa3.1 channel blockade on tumor growth in vivo was also studied using xenograft model in nude mice. Results: The protein expression of KCa3.1 channel was upregulated in ICC tissues and was correlated with age, lymph node metastasis and TNM stage. And high KCa3.1 expression indicated a worse prognosis in ICC patients. Blocking KCa3.1 channel with a specific inhibitor TRAM-34 reduced the proliferation and invasion of ICC cells. Knockdown of KCa3.1 could achieve the same effects through decreasing NF-κB activation. Further in vivo studies demonstrated that KCa3.1 channel blockade suppressed ICC tumor growth. Conclusions: Our observations suggested KCa3.1 might be a promising novel therapeutic target in intrahepatic cholangiocarcinoma.

Bile deficiency induces changes in intestinal glucose absorption in mice.

BACKGROUND: Biliary tract obstruction is a common clinical problem. In this study, we attempted to understand the change in intestinal glucose absorption after biliary tract obstruction. METHODS: Experimental models of murine biliary duct ligation and external biliary drainage were established. Murine intestinal mucosal glucose absorption was examined with Ussing chambers according to the increase in the short-circuit current in vitro and blood glucose measurement after oral glucose in vivo. The protein expression of the sodium-glucose cotransporter (SGLT1) and the facilitated glucose transporter, member 2 (GLUT2) was analyzed by Western blot and immunohistochemistry. RESULTS: The results from Ussing chamber experiments showed that duodenal mucosal glucose absorption levels were significantly higher in biliary duct ligation and biliary drainage mice than those in normal control mice at 1 and 2 weeks after the operation. Gastrointestinal bile acid administration almost reversed the elevated duodenal mucosal glucose absorption to the normal level in biliary drainage mice. The results from the experiments in vivo further confirmed that the glucose absorption increased in biliary duct ligation and biliary drainage mice. The protein expression levels of SGLT1 in the duodenal mucosae of both biliary duct ligation and biliary drainage mice were markedly higher than those in control mice, and the protein expression of GLUT2 was not significantly altered, compared with control mice. CONCLUSION: Bile deficiency in the intestine upregulates the expression of intestinal mucosal SGLT1 and enhances intestinal mucosal glucose absorption capacity, which contributes to the understanding of intestinal physiologic function for patients with biliary duct obstruction and external biliary drainage.