Carbapenem-resistant Klebsiella pneumoniae (CRKP) strains pose a significant threat to public health. In this study, a survey was conducted in the Jiangxi Province of China, covering a total of 140 CRKP strains collected from 11 hospital laboratories from June 2016 to January 2018. All CRKP isolates were subjected to antimicrobial susceptibility testing, capsular serotypes, virulence gene profiles, multilocus sequence typing, and pulsed-field gel electrophoresis. The differences in the patient characteristics and distributions among the various regions were statistically significant ( p ≤ 0.001). Most patients were hospitalized in intensive care units (30.0%) and burn departments (13.6%), with lower respiratory (52.1%) and urinary tract (15.7%) infections being most prevalent. A higher ratio of CRKP isolates were identified in the southern and central regions of Jiangxi than in the other regions. Only two carbapenemase genes, bla _KPC and bla _NDM , were responsible for phenotypic resistance in the tested CRKP strains (46.5% and 22.1%, respectively), among which several major sequence types (STs), such as ST11 (27.8%) and ST23 (14.8%), were identified. A total of 39 virulent strains were detected, of which 22 strains were classified by capsule serotyping. Hypervirulent genes were most common in the eastern and central regions of Jiangxi. In conclusion, CRKP strains in the Jiangxi Province have varied geographic distributions; the resistance rates of isolates harboring bla _KPC decreased from southern to northern regions, whereas the drug resistance gene bla _NDM showed a tendency to spread from a central point to the surrounding areas. ST23 carbapenem-resistant hypervirulent K. pneumoniae is emerging, resulting in an urgent need to enhance clinical awareness.

Acute infectious urticaria, a subset of acute urticaria, with severe persistence wheals and systemic symptoms, response well to corticosteroids treatment in combination with antibiotics. The exact pathogenic mechanisms are not fully understood. In this study, we aim to analyze the different clinical features, compare the level of neutrophil activation, and investigate the expression of inflammatory related cytokine in patients with acute urticaria and acute infectious urticaria. Eighteen patients with acute infectious urticaria and eighteen patients with acute urticaria were included in this study. We analyzed the difference between the clinical features and the serum expressions of pro-inflammatory factors in the two groups, then examined the levels of inflammation-associated cytokines before and after treatment of acute infectious urticaria. Hematoxylin & eosin (HE) staining and immunohistochemistry (IHC) were used to further study the relationship between neutrophil and neutrophil-derived Myeloperoxidase (MPO) of lesions in the two groups. The expression levels of C-reactive protein (CRP), D-dimer, interleukin 6 (IL-6), IL-8 and chemokine ligand 8 (CCL8) in serum were significantly higher in acute infectious urticaria than acute urticaria. In acute infectious urticaria, the serum expression levels of CCL8 were significantly decreased after the treatment, a significant correlation observed between CRP levels and IL-6, both CCL8 and CRP were positively correlated with neutrophil granulocytes. Neutrophils infiltration were not observed by HE stains in two groups, but in IHC stains we found a positive expression of MPO in acute infectious urticaria lesions. Elevated neutrophil in the serum, which is associated with the levels of IL-8 & CCL8, and positively expressed MPO in lesions, may be involved in the pathogenic mechanism of acute infectious urticaria.

Cutaneous melanoma is a highly aggressive and malignant skin cancer, and its high recurrence rate and drug resistance increase the difficulty of treating advanced-stage patients. Studies have revealed that treatment via stimulation of alpha-1 adrenergic receptor (ADRA1) subtypes inhibits melanoma growth in mice. However, the associations between alpha-1D adrenergic receptor (ADRA1D) and cutaneous melanoma are poorly understood. Tissue specimens from 16 pairs of patients with a pigmented nevus and cutaneous melanoma were analyzed for ADRA1D expression using immunohistochemical staining. Western blotting and RT-qPCR were carried out in order to detect ADRA1D expression levels in melanoma cells and human epidermal melanocytes (HEMs), hypoxia-inducible factor-1α (HIF-1α), and vascular endothelial growth factor (VEGF) levels in HUVECS. A375 cells were transfected with a lentivirus overexpressing ADRA1D. Wound-healing, Transwell, and cell proliferation assays were utilized to identify the ADRA1D effect on the migration, invasion, and proliferation of the two groups of A375 cells in vitro. In order to evaluate the function of ADRA1D in vivo, a melanoma xenograft model was developed in immunodeficient mice. ADRA1D was low expressed in cutaneous melanoma tissues. Overexpression of ADRA1D inhibited the tubulation and migration of HUVECs in vitro. Overexpression of ADRA1D significantly decreased the HIF-1α and VEGF expression. Overexpression of ADRA1D inhibited the invasion and proliferation of A375 melanoma cells in vitro and reduced its angiogenesis in vivo. ADRA1D inhibits cutaneous melanoma growth and angiogenesis. It attenuates melanoma cell proliferation and invasion. Meanwhile, its anti-angiogenic effect is achieved by negatively regulating the HIF-1α/VEGF axis in melanoma tissue, thereby attenuating the growth of cutaneous melanoma and reducing the potential of metastasis.