Castleman Disease Presenting in the Neck: A Report of 3 Cases and a Literature Review.

BACKGROUND Castleman's disease (CD) is a reactive lymph node hyperplasia initially identified by Castleman in 1956. CD predominantly affects individuals 20-50 years of age, with low incidence in children. This case report describes 3 cases of CD treated in our hospital and reviews the relevant literature. The purpose of this case report was to enhance clinical understanding and treatment of CD in the head and neck in children. CASE REPORT To enhance clinical understanding and improve treatment of CD in the head and neck region in children, we present the cases of 3 patients who were admitted to the hospital, primarily presenting with a neck mass. Preoperatively, the patients collectively exhibited non-specific findings. Surgical interventions were performed with Cases 1 and 3 undergoing left functional (radical) neck lymph node dissection, in contrast to Case 2, in which bilateral functional (radical) neck lymph node dissection was executed. Pathological examination confirmed the diagnosis of CD in each of the 3 patients. Following surgery, a follow-up period ranging from 3 months to 1 year revealed that all patients had successfully recovered, with no recurrence. CONCLUSIONS Castleman disease is a rare disease in children and difficult clinical diagnosis. Some patients with unicentric Castleman disease (UCD) can be treated with surgery, and those with multicentric Castleman disease (MCD) need chemotherapy, but at present there is no widely accepted treatment plan.

SNHG15 enhances cisplatin resistance in lung adenocarcinoma by affecting the DNA repair capacity of cancer cells.

BACKGROUND: Lung adenocarcinoma (LUAD) is a prevalent malignancy. SNHG15 has been demonstrated to be oncogenic in many kinds of cancers, however the mechanism of SNHG15 in LUAD cisplatin (DDP) resistance remains unclear. In this study, we demonstrated the effect of SNHG15 on DDP resistance in LUAD and its related mechanism. METHODS: Bioinformatics analysis was adopted to assess SNHG15 expression in LUAD tissues and predict the downstream genes of SNHG15. The binding relationship between SNHG15 and downstream regulatory genes was proved through RNA immunoprecipitation, chromatin immunoprecipitation and dual-luciferase reporter assays. Cell counting kit-8 assay was adopted to evaluate LUAD cell viability, and gene expression was determined by Western blot and quantitative real-time polymerase chain reaction. We then performed comet assay to assess DNA damage. Cell apoptosis was detected by Tunnel assay. Xenograft animal models were created to test the function of SNHG15 in vivo. RESULTS: SNHG15 was up-regulated in LUAD cells. Moreover, SNHG15 was also highly expressed in drug-resistant LUAD cells. Down-regulated SNHG15 strengthened the sensitivity of LUAD cells to DDP and induced DNA damage. SNHG15 could elevate ECE2 expression through binding with E2F1, and it could induce DDP resistance by modulating the E2F1/ECE2 axis. In vivo experiments verified that the SNHG15 could enhance DDP resistance in LUAD tissue. CONCLUSION: The results suggested that SNHG15 could up-regulate ECE2 expression by recruiting E2F1, thereby enhancing the DDP resistance of LUAD.

Methylprednisolone accelerate chest computed tomography absorption in COVID-19: A three-centered retrospective case control study from China.

BACKGROUND: Based on the results of some large randomized controlled trials (RCTs) confirmed the efficacy of corticosteroids in coronavirus disease 2019 (COVID-19), corticosteroids have been included in World Health Organization guidelines, but remain controversial. AIM: To investigate the efficacy and safety of low-to-moderate dose (30 to 40 mg/d) short-term methylprednisolone for COVID-19 patients. METHODS: The clinical data of 70 patients diagnosed with COVID-19 who received antiviral therapy with Arbidol for 7-10 d before admission but had no obvious absorption on chest computed tomography (CT) imaging were retrospectively analyzed. Arbidol (as the control group) and methylprednisolone (as the corticosteroid group) were given respectively after admission. After treatment, chest CT was reexamined to evaluate the absorption of pulmonary lesions. Additionally, we evaluated and compared the lymphocyte count, erythrocyte sedimentation rate (ESR), interleukin-6(IL-6), serum ferritin, lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB), hypersensitive C-reactive protein (hs-CRP) and D-dimer levels, and also analyzed the incidence of toxic and side effects. RESULTS: All patients in the corticosteroid group had varying degrees of CT absorption, which was significantly better than that in the control group (CT obvious absorption rate: 89.47% vs 12.5%, P < 0.05). The average daily dose and course of methylprednisolone in the patients with significant improvement on chest CT was (38.55 ± 13.17) mg and (6.44 ± 1.86) d respectively. During the treatment, the lymphocyte count, ESR, IL-6, serum ferritin, LDH, CK-MB, hs-CRP and D-dimer levels all improved gradually, indicating that both Arbidol and methylprednisolone therapy were contributed to improving the condition of COVID-19 patients. The corticosteroid regimen did not prolong the clearance time of severe acute respiratory syndrome coronavirus 2. There were no severe adverse reactions such as gastrointestinal bleeding, secondary severe infection, hypertension, diabetic ketoacidosis, mental disorders or electrolyte disorders during the whole corticosteroid treatment process. CONCLUSION: Low-to-moderate dose short-term methylprednisolone can accelerate the chest CT imaging absorption of COVID-19 so as to improve symptoms and alleviate the condition in a short term, reduce the hospital stay, meanwhile avoid severe COVID-19 phases. The protocol has been proven to be effective and safe in clinical use.

Successful treatment of gastrointestinal infection-induced septic shock using the oXiris® hemofilter: A case report.

BACKGROUND: Septic shock leads to multiple organ failure, and bacterial endotoxins and endogenous cytokines play essential roles in the pathogenesis. The oXiris® hemofilter can efficiently adsorb endotoxins and cytokines. CASE SUMMARY: We admitted a critically ill 59 year-old male patient with gastrointestinal septic shock due to infection by a Gram-negative bacterium and septic acute kidney injury (AKI). Prior to intensive care unit admission, the patient reported intermittent diarrhea and decreased urine output. His blood pressure was 70/40 mmHg, necessitating fluid resuscitation and large doses of noradrenaline. Based on the results of a blood culture and the presence of hypotension, oliguria, and hypoxemia, we diagnosed septic shock, AKI, and multiple organ dysfunction. We administered continuous renal replacement therapy (CRRT) with an oXiris® hemofilter for 72 h with intermittent continuous veno-venous hemodiafiltration (CVVHDF), and changed the filter every 12 h. After his hemodynamic parameters were stable, we used a traditional filter (AN69 hemofilter) with intermittent CVVHDF. The 72 h CRRT with the oXiris® hemofilter led to stabilization of his vital signs, marked reductions in disease severity scores, and decreased levels of procalcitonin, endotoxin, and inflammatory factors. After 8 d of CRRT, his kidney function had completely recovered. CONCLUSION: We conclude that the oXiris® hemofilter combined with appropriate antibacterial therapy was an effective treatment for this patient with gastrointestinal septic shock.

Patient pathway analysis of tuberculosis diagnostic delay: a multicentre retrospective cohort study in China.

OBJECTIVES: Delay in diagnosis of tuberculosis (TB) is an important but under-appreciated problem. Our study aimed to analyse the patient pathway and possible risk factors of long diagnostic delay (LDD). METHODS: We enrolled 400 new bacteriologically diagnosed patients with pulmonary TB from 20 hospitals across China. LDD was defined as an interval between the initial care visit and the confirmation of diagnosis exceeding 14 days. Its potential risk factors were investigated by multivariate logistic regression and multilevel logistic regression. Hospitals in China were classified by increasing size, from level 0 to level 3. TB laboratory equipment in hospitals was also evaluated. RESULTS: The median diagnostic delay was 20 days (IQR: 7-72 days), and 229 of 400 patients (57.3%, 95%CI 52.4-62.1) had LDD; 15% of participants were diagnosed at the initial care visit. Compared to level 0 facilities, choosing level 2 (OR 0.27, 95%CI 0.12-0.62, p 0.002) and level 3 facilities (OR 0.34, 95%CI 0.14-0.84, p 0.019) for the initial care visit was independently associated with shorter LDD. Equipping with smear, culture, and Xpert at initial care visit simultaneously also helped to avoid LDD (OR 0.28, 95%CI 0.09-0.82, p 0.020). The multilevel logistic regression yielded similar results. Availability of smear, culture, and Xpert was lower in level 0-1 facilities than in level 2-3 facilities (p < 0.001, respectively). CONCLUSIONS: Most patients failed to be diagnosed at the initial care visit. Patients who went to low-level facilities initially had a higher risk of LDD. Improvement of TB laboratory equipment, especially at low-level facilities, is urgently needed.

Tripchlorolide induces autophagy in lung cancer cells by inhibiting the PI3K/AKT/mTOR pathway and improves cisplatin sensitivity in A549/DDP cells.

Tripchlorolide (T4) has been shown to induce A549 lung cancer cell death predominantly by activating an autophagy pathway. However, the underlying mechanism remains unclear. Herein, we demonstrated that compared with T4 treatment alone, pretreatment with wortmannin (an inhibitor of phosphatidylinositol 3-kinase), perifosine (an inhibitor of AKT) or rapamycin (an inhibitor of mTOR) combined with a subsequent T4 treatment significantly impaired the cell viability of A549 and A549/DDP lung cancer cells. We found that either treatment scheme markedly reduced the activity of P13K and AKT. Expression of LC3II increased in parallel to the increase of the T4 concentration in both A549 and A549/DDP cells and was repressed by overexpression of AKT. The expression levels of PI3-K, PI3-P, AKT, TSC2, mTOR, p70S6K and 4E-BP1 were minimally affected by the wortmannin, perifosine, or rapamycin plus T4 treatments, but their phosphorylated products were greatly affected in A549 lung cancer cells and slightly affected in A549/DDP lung cancer cells. These results indicate that T4 induces autophagy in lung cancer cells by inhibiting the PI3K/AKT/mTOR signaling pathway. We further found that T4 decreased expression of MDR1 and improved cisplatin sensitivity of A549/DDP cells. Altogether, these results have meaningful implications for tumor therapy in the future.