Giant pulmonary bullae mistaken for pneumothorax.

Differentiating between giant pulmonary bullae and pneumothorax can pose a challenge in clinical settings. A chest CT scan during the patient's health assessment revealed that approximately 40% of the right chest cavity was filled with air, leading to incomplete expansion of the right lung. The patient was initially misdiagnosed with pneumothorax in the emergency department and subsequently underwent closed thoracic drainage without experiencing any improvement in symptoms. Upon further examination through thoracoscopy, the patient was correctly diagnosed with a giant pulmonary bulla. Upon reviewing the patient's chest CT scan, we were able to identify key distinguishing features between giant pulmonary bullae and pneumothorax.

Correlation between catheter colonization of central venous catheters and clinical biochemical indicators: A retrospective analysis of the MIMIC­IV database.

BACKGROUND: Clinical studies have not fully assessed the potential impact of patients' biochemical indicators on the rate of positive for central venous catheter-tip microorganism culture (PCMC). METHODS: Data were obtained from an online Medical Information Mart for Intensive Care IV database. Patients who were ≥18 years old and had central venous catheter-tip culture results without continuous renal replacement therapy were included in the study. A comparison of patient characteristics and their biochemical indicators was made between negative and positive culture results. RESULTS: A total of 5,323 patients were included in the analysis, including 612 positive (PCMC group) and 4,711 negative culture results (negative for central venous catheter tip catheter-tip microorganism culture [NCMC] group). The only influence factor on PCMC in this study was the serum creatinine (Scr) (odds ratio: 1.312, 95% confidence interval: 1.084-1.590, P = .005), according to a binary logistic regression analysis. The cut-off value of Scr was 3.25 mg/dL. The prevalence of PCMC (27.1% vs 9.1%, P < .001) and Staphylococcus aureus (43.0% vs 18.6%, P < .001) for central venous catheter-tip culture results was much higher in patients with Scr ≥ 3.25 mg/dL than those Scr < 3.25 mg/dL. CONCLUSIONS: We used the large dataset collected from Medical Information Mart for Intensive Care IV to show that patients with Scr ≥ 3.25 mg/dL had an increased risk for PCMC.

Massive hemorrhage from an aortoesophageal fistula caused by esophageal stent implantation: A case report and literature review.

RATIONALE: Aortoesophageal fistula (AEF) is the direct communication between the aorta and esophagus, which can cause fatal hemorrhage, and its incidence increased with the use of an esophageal stent (ES). PATIENT CONCERNS: A 79-year-old man was admitted due to hemodynamic shock with massive hematemesis caused by AEF 1 month after the implantation of an ES. DIAGNOSES: Computed tomography angiography visualized an AEF with an ulcer-like projection on the aortic arch where the ES was placed. Angiography of the aorta revealed extravasation of contrast media from the aortic arch into the stented esophagus, which confirmed the diagnosis. INTERVENTIONS: Thoracic endovascular aortic repair (TEVAR) was performed for massive hematemesis caused by ES-related, AEF but did not solve the underlying problem, leading to the second fatal hemorrhage. LESSONS: TEVAR for the unique treatment of ES-related AEF is feasible in certain cases but may lead to collapse after a specific period.

Inhibition of microRNA-183 expression resists human umbilical vascular endothelial cells injury by upregulating expression of IRS1.

Our study aims to investigate the effect of microRNA-183 (miR-183) on human umbilical vascular endothelial cells (HUVECs) injury by targeting IRS1. HUVECs injury was induced by oxidized low-density lipoprotein (ox-LDL). HUVECs were grouped so as to explore the role of ox-LDL and miR-183 in HUVECs injury, with the expression of miR-183 and IRS1 detected. Additionally, the related factors of oxidative stress and inflammation, as well as angiogenesis ability, proliferation, cell cycle, apoptosis, invasion, and migration abilities were also measured. Ox-LDL treatment could decrease the activity of HUVECs, increase the level of oxidative stress and inflammation, and induce the HUVECs injury. miR-183 could inhibit the expression of IRS1. The inhibition of miR-183 expression in ox-LDL-induced HUVECs injury could enhance cell activity, inhibit inflammatory level, and thus resist cell injury. Low expression of IRS1 could reverse the inhibition of miR-183 on HUVECs injury. This study highlights that inhibition of miR-183 expression may resist HUVECs injury by upregulating expression of IRS1.

Characterization of ciprofloxacin-resistant and ESBL-producing Salmonella enteric serotype Derby in Eastern China.

BACKGROUND: Fluoroquinolone resistance and ESBL-production are concurrently found in a limited number of Salmonella serotypes. The present study was aimed to characterize fluoroquinolone-resistant and ESBL-producing Salmonella enteric serotype Derby (S. Derby) isolates in terms of antimicrobial susceptibility, relevant genetic mechanisms, and PFGE. RESULTS: From 2013 to 2017 in Ningbo China, 52 S. Derby isolates were identified out of 826 non-typhoidal Salmonella isolates from patient feces, food, and environmental water samples. Three S. derby isolates were identified to be fluoroquinolone-resistant and ESBL-producing with cefotaxime MIC of 64 µg/mL and ciprofloxacin MIC of 4 µg/mL. The three isolates contained the same genetic structure of quinolone resistance, including a silent gyrA mutation S (TCC) 83S (TCT) and three PMQR genes qnrB, qnrS and aac(6')-Ib-cr. As withß-lactams resistance mechanisms, two isolates contained blaTEM, blaOXA, and blaCTX-M genes and one isolate contained blaOXA and blaCTX-M genes. Additionally, two isolates displayed more identical PFGE pattern than the third isolate, whereas three isolates showed the same plasmid profile of I1, W and P by PCR-based replicon typing. The conjugation experiment showed no dissemination of ß-lactam resistance by direct contact among isolates; the transformation experiment failed to transfer plasmid conferring ampicillin resistance to E. coli DH5a. CONCLUSION: The present study demonstrates the emerging fluoroquinolone-resistant and ESBL-producing S. Derby in both humans and the environment. Seeing that S. Derby has become one of the most common Salmonella serotypes, this situation gives rise to a new major risk of food-borne diseases.

Relation Between Superficial Calcifications and Plaque Rupture: An Optical Coherence Tomography Study.

BACKGROUND: There are several forms of calcium deposition, which play different roles in the stability of the coronary artery. It remains unknown whether certain calcification morphological characteristics determine rupture of lipid-rich lesions in the same plaque in acute coronary syndrome (ACS). METHODS: We retrospectively analyzed 550 patients with ACS between May 2008 and October 2014, who had undergone preintervention optical coherence tomography (OCT) imaging examination. A total of 78 patients with 78 culprit lipid-rich lesions having superficial calcifications on OCT images were included in this study, among which 45 were ruptured lesions with calcium and 33 were nonruptured lipid-rich lesion with calcium. The smallest depth of calcium (CAL-DEP) was determined, and the morphology of the calcifications and plaques was analyzed during preintervention OCT imaging. RESULTS: The CAL-DEP was significantly thinner in ruptured lesions with calcium than in nonruptured lipid-rich lesion with calcium (median, 50 [interquartile range (IQR), 33-63] µm vs 110 [73-208] µm; P < 0.001) and in myocardial infarction than in unstable angina pectoris patients (median, 57 [IQR, 36-78] µm vs median, 85 [IQR, 43-140] µm; P = 0.045). For lipid-rich calcified plaques, when CAL-DEP was < 63 µm, the lipid-rich lesion was most vulnerable and prone to rupture (sensitivity = 77.8%; specificity = 81.8%; area under the curve: 0.804; P < 0.0001). CONCLUSIONS: Small CAL-DEP in lipid-rich calcified plaques is a morphological characteristic of a vulnerable plaque phenotype. A CAL-DEP ≤ 63 µm is the critical depth of calcification for lipid-rich calcified plaque rupture in patients with ACS.

Statin-induced improvements in vulnerable plaques are attenuated in poorly controlled diabetic patients with coronary atherosclerosis disease: a serial optical coherence tomography analysis.

AIMS: The incidence of cardiac events is increased in diabetic patients even after lipid-lowering therapy. This study aimed to compare the statin-induced changes in the characteristics of vulnerable plaques in patients without diabetes mellitus (DM) and in those with better- or poorly controlled DM, measured by optical coherence tomography (OCT). METHODS: This was a retrospective study of 99 non-culprit lipid-rich plaques from 75 patients who underwent intensive OCT imaging examination. Thirty-four non-diabetic patients were assigned to Group A. According to the average HbA1c level, 22 diabetic patients were assigned to Group B, and 19, to Group C (average HbA1c < 8 and ≥8 %, respectively). RESULTS: Following 12 months of statin therapy, similar improvements in serum lipid levels were observed in the three groups. However, the increase in fibrous-cap thickness of plaques was the highest in Group A (Group A, 183 %; Group B, 104 %; and Group C, 53 %). Significant reductions in lipid volume index were observed in Groups A and B (Group A: -12 %, P < 0.001; Group B: -13 %, P = 0.038; Group C: 7 %, P = 0.948). Percent changes in OCT measurements were significantly correlated with average HbA1c in patients. CONCLUSIONS: Improved glucose control may enhance the statin-induced reduction in characteristics of vulnerable plaque in diabetic patients.