Case report: Preliminary study on the diagnosis and treatment of respiratory distress in patients with giant nodular goiter complicated with severe COVID-19.

Background: To investigate the practicality of emergency surgical and conservative medical treatments in patients with giant nodular goiter complicated by severe coronavirus disease 2019 (COVID-19)-related respiratory distress, evaluate the prognosis based on the two interventions, and explore the diagnosis and treatment plan of COVID-19-related respiratory distress in patients with giant nodular goiter. Methods: Four cases were retrospectively collected. Among them, two cases underwent emergency surgery, one case was treated with conservative treatment, whereas the fourth case underwent emergency surgery after failure of conservative therapy. Results: Dyspnea was significantly improved postoperatively, and the endotracheal tube was successfully removed 10.5 h after the operation, but inflammatory markers were greatly enhanced as compared to the preoperative values, patients with different degrees of fever, cough, and other discomforts postoperatively. Case 1 showed complete remission of all symptoms after 3 weeks, while case 2 displayed fever, cough, drowsiness, and other symptoms after the discharge and was eventually readmitted. In case 3, the conservative COVID-19 treatment marginally improved the pulmonary infection, fever, and other symptoms, but cough and other discomforts were persistent, along with delirium in later stages. Moreover, case 4 reported extubation failure after undergoing treatment with the standard new coronary pneumonia regimen in the tracheal intubation state; however, the patient was successfully weaned and extubated 9 days after emergency surgery to relieve the obstruction. Conclusion: Our preliminary exploration suggested that patients with giant nodular goiter and respiratory tract obstruction post-acute COVID-19 infection can undergo early surgery after surgical tolerance evaluation for a better prognosis.

Downregulation of miR-4284 can inhibit the apoptosis of Human Arterial Smooth Muscle Cells (HASMCs) in arteriosclerosis obliterans (ASO).

Introduction The disease arteriosclerosis obliterans (ASO) affects the lower extremities. ASO's mechanism involves the proliferation and migration of vascular smooth muscle cells (VSMCs). The miR-4284 is involved in several biological processes of the cardiovascular system, including VSMC proliferation, migration, and death. However, it is unknown if the miR-4284 gene is involved in the control of ASO. Furthermore, the molecular processes behind the contribution of human arterial smooth muscle cells (HASMCs), one of the most significant components of the arterial wall, to arteriosclerosis obliterans (ASO) pathogenesis remain unknown. Previously, we explored the alterations of miRNAs in the blood of ASO patients, and now we wanted to test further whether these changes also take place in the HASMCs that are responsible for the pathogenesis of ASO. Methods The expression levels of miR-29a in arterial walls were analyzed via a real-time polymerase chain reaction. An ASO cell model was established to investigate the expression of miR-4284 on HASMCs. The Transwell system and CCK-8 detection were used to assess the migration and proliferation of HASMCs. The proportion of apoptotic cells as well as the concentrations of apoptotic signal protein production were assessed using flow cytometry. A Western blot technique was used to identify B cell lymphoma-2 (Bcl2), Bcl2-associated X protein (BAX), as well as X-linked inhibitors of apoptosis protein (XIAP). Results The results showed that PCR confirmed that the qualified production or expression of miR-4284 was significantly reduced in HASMCs after they were cultured without FBS and in an atmosphere of 1% O2 + 5% CO2 + 94% N2 and that glucose had no effect on its expression. MiR-4284 has no effect on migration and proliferation, but downregulation of miR-4284 can decrease the apoptotic rate of HASMCs, as revealed by flow cytometry. Furthermore, western blot experiments showed that the expression of BAX was low, while the expression of the other two proteins, viz., Bcl2 and XIAP, was over-expressed. Conclusion We found that miR-4284 downregulation enhanced Bcl2, as well as XIAP, and decreased Bax. This shows that downregulated miR-4284 regulates apoptosis-related protein expression in HASMCs. The mechanism is not clear, and we need further study to confirm it.

Long noncoding RNA LINC00857 promotes pancreatic cancer proliferation and metastasis by regulating the miR-130b/RHOA axis.

Dysregulation of long noncoding RNAs (lncRNAs) is involved in the pathogenesis and progression of pancreatic cancer (PC). In the current study, we investigated the role and molecular mechanism of LINC00857 in PC. The expression of LINC00857 in PC was analyzed by bioinformatics analysis and qRT-PCR, and the relationship between LINC00857 expression and clinical characteristics of patients of PC was analyzed by Fisher's exact test. Gain- and loss-of-function assays were performed to determine the biological function of LINC00857 in PC. The relationship between LINC00857, miR-130b, and RHOA were determined by RNA pull-down assay, luciferase assay, and qRT-PCR. Our results demonstrated that LINC00857 expression was elevated in PC, and high expression of LINC00857 was positively associated with tumor diameter, T stage, and lymph node metastasis. LINC00857 promoted the proliferation and mobility of PC cells in vitro and in vivo. Mechanistically, LINC00857 acts as a sponge for miR-130b and decreases its expression. miR-130b exhibits tumor suppressor functions in PC, and RHOA was identified as the key target gene of miR-130b. The functions induced by LINC00857 in PC cells were dependent on the miR-130b/RHOA axis. In conclusion, the current study indicated that LINC00857 promotes PC tumorigenesis and metastasis by modulating the miR-130b/RHOA axis, implying that LINC00857 might be a new therapeutic target for PC.

Prophylaxis of neutropenia with mecapegfilgrastim in patients with non-myeloid malignancies: a real-world study.

BACKGROUND: Chemotherapy-induced neutropenia is commonly encountered in clinical practice. The management of neutropenia has been evolving from short-acting granulocyte colony-stimulating factors (G-CSFs) to long-acting G-CSFs. However, an evaluation of the safety and effectiveness of long-acting G-CSFs in clinical practice is still lacking. METHODS: This multicenter, non-interventional study was aimed at exploring the safety and effectiveness of mecapegfilgrastim in different cancer patients in China. All patients provided written informed consent prior to the study and were treated according to routine clinical practice. Different prophylactic strategies (primary or secondary prophylaxis) were also compared. RESULTS: This study included 638 patients from May 2019 to November 2020. More than half of the participants were breast cancer patients. The mean age of all the patients was 56 years. White blood cell increase (6.2%) was the most frequently reported adverse event (AE) possibly related to the study drug. No unexpected AEs were reported. Grade ≥3 neutropenia in chemotherapy treatment cycle 1 was reported in 36 (5.6%) patients. Incidence of grade ≥3 neutropenia in cycle 1 in the primary and secondary prophylaxis subgroups were of 4.3% and 9.2%, respectively. A decreasing trend of severe neutropenia incidence was observed from cycle 1 to cycle 4. CONCLUSIONS: Mecapegfilgrastim was generally well tolerated, and no unexpected AEs were observed in this study. Primary administration of mecapegfilgrastim led to a lower incidence of neutropenia than did secondary administration. Continuous administration of mecapegfilgrastim could keep the incidence of neutropenia to a relatively low level.

Modified autologous adipose transplantation in the treatment of depressed scars: an experimental study.

OBJECTIVE: Complex depressed scars can cause tissue adhesion, resulting in serious joint dysfunction. In recent years, autologous adipose and adipose-derived stem cells have been widely used to treat depressed scars, but there are still limitations in these treatment that should be resolved. This study aimed to investigate the therapeutic effects of adipose tissues collected with modified technique on the depressed scars in animals. METHODS: The adipose tissues were collected with a forward technique, and tissue viability in vitro and the survival of transplanted tissues in in nude mice were further assessed. Furthermore, the therapeutic effects of adipose tissues collected with new technique and traditional technique on the depressed scars were explored in an animal model of bleomycin induced scar formation. RESULTS: The adipose tissues collected with the new technique had a higher glucose transport (P<0.01); after transplantation into the nude mice, the amount of residual tissues and the survival rate in the modified group were higher than in the traditional group (P<0.05); electron microscopy showed the intercellular space was covered with reticular structure, in which there was a large amount of microvessel structure in the adipose tissue of the modified group; immunohistochemistry showed that the microvessel density (MVD) in the modified group increased significantly (P<0.01). At 28 d after transplantation into the scar animals, the dermal collagen fibers became thicker and showed regular arrangement, the myofibroblasts became regenerative and inflammation was improved as compared to blank control group. In the untreated scar group, the collagen fibers were loose and irregular, and a large amount of inflammatory cells was observed. In addition, the dermal expression of α-SMA and TGF-ß1 in the transplantation group reduced significantly as compared to scar group (P<0.05). CONCLUSION: The autologous adipose tissues collected with the new technique possess higher activity ad contain more. In scar animals, transplantation of these adipose tissues may improve the scar structure and inhibit the scar formation which may be related to the suppressed expression of α-SMA and TGF-ß1.