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The present case reports on a 53-year-old patient with severe chronic obstructive pulmonary disease (COPD) and acute pneumonia who complained of massive right-sided chest pain and hemoptysis after a severe coughing fit. To the authors' great surprise, further clinical and radiological investigations revealed a rupture of the right intercostal muscles caused by the coughing fit, with herniation of parts of the right lower lobe of the lung down to the subcutaneous and below the M. latissimus dorsi. The patient was presented to the colleagues in thoracic surgery and needed to be operated twice, finally with a mesh insert.

Interstitial cystitis/bladder pain syndrome with Hunner's lesion (HIC) is characterized by chronic inflammation and nerve hyperplasia; however, the pathogenesis of HIC remains a mystery. In this study, we detected both EBV latency infection genes EBNA-1, LMP-1, and EBV lytic infection BZLF-1 and BRLF-1 expression in the HIC bladders, indicating coexistence of EBV persistence and reactivation in the B cells in HIC bladders. Upregulation of EBV-associated inflammatory genes in the HIC bladders, such as TNF-α and IL-6, suggests EBV infection is implicated in the pathogenesis of bladder inflammation. Nerve hyperplasia and up-regulation of brain-derived neurotrophic factor (BDNF) were noted in the HIC bladders. Double immunochemical staining and flow cytometry revealed the origin of BDNF should be the EBV infected B cells. Inducible BDNF expression was noted in B cells upon EBV infection, but not in the T cells. Chromatin immunoprecipitation study revealed BDNF transcription could be promoted by a cooperation between EBV nuclear antigens, chromatin modifiers, and B cell specific transcription. Knockdown of BDNF in EBV infected B cells resulted in inhibition of cells proliferation and viability. Downregulation of phosphorylated SMAD2 and STAT3 after BDNF knockdown may play a role in the mechanism. Implantation of latent EBV infected B cells into rat bladder walls resulted in higher expression level of CD45 and PGP9.5, suggesting tissue inflammation and nerve hyperplasia. In contrast, implantation of BDNF depleted EBV infected B cells abrogated these effects. This is the first study to provide insights into the mechanisms underlying the involvement of EBV infected B cells in HIC pathogenesis. This article is protected by copyright. All rights reserved.

To assess prevalence of central sensitization (CS) and its association with demographic and clinical factors in patients with endometriosis.

Postoperative pain is one of the main negative symptoms resulting from surgery and the use of new methods to control this symptom is of ever-increasing relevance. Opioid-sparing strategies, such as multimodal analgesia, are trends in this scenario. Pregabalin is a well-established treatment for neuropathic pain; however, it is still controversial in the surgical context for postoperative analgesia. The aim of this study was to investigate the effect of pregabalin on postoperative analgesia in patients undergoing abdominal hysterectomy.

Complex regional pain syndrome (CRPS) is marked by disproportionate pain after trauma. While long-term outcome is crucial to patients, predictors or biomarkers of the course of pain or CRPS symptoms are still lacking. In particular, microRNAs, such as miR-223, decreased in CRPS, have been described only in cross-sectional studies.

Eugenia gracillima is widely used by the population in the manufacture of pulps and jellies, with popular reports of its use in the treatment of infections in the urinary system, respiratory and dermatological problems. A previous study reports that EO from E. gracillima leaves proved to be a promising antioxidant agent in combating the promastigote forms of protozoa. Despite this, this species has been little studied due to its pharmacological properties.

Sorafenib-resistance leads to poor prognosis and high mortality in advanced hepatocellular carcinoma (HCC), and this study aims to investigate the functional role of a circular RNA ITCH (circITCH) in regulating the sorafenib-resistance of HCC and its underlying mechanisms.

The amyloid precursor protein (APP) is critical for the pathogenesis of Alzheimer's disease (AD). The AD patients usually have lower pain sensitivity in addition to cognitive impairments. However, considerably less is known as yet about the role of APP and its two mammalian homologues, amyloid precursor-like protein 1 and 2 (APLP1, APLP2), in spinal processing of nociceptive information. Here we found that all APP family members were present in spinal cord dorsal horn of adult male C57BL/6J mice. Peripheral nerve injury specifically reduced the expression of spinal APLP2 that correlated with neuropathic mechanical allodynia. The loss of APLP2 was confined to inhibitory GABAergic interneurons. Targeted knockdown of APLP2 in GABAergic interneurons of GAD2-Cre mice evoked pain hypersensitivity by means of microglia activation. Our data showed that GABAergic terminals expressed APLP2, a putative cell adhesion protein that interacted with microglia-specific integrin molecule CD11b. Knocking down APLP2 in GAD2-positive neurons to disrupt the trans-cellular interaction led to microglia-dependent pain sensitization. Our data thus revealed an important role of APLP2 for GABAergic interneurons to control microglial activity and pain sensitivity.

There are limited real-world data about patient-reported outcomes with immunotherapies (IO) in metastatic non-small cell lung cancer (mNSCLC). We describe patient-reported distress and clinical outcomes with IO-based treatments or cytotoxic chemotherapies (Chemo).