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Potassium iodide (KI), initially derived from seaweed in the early 19th century, is used for treating sporotrichosis in dermatological practice. KI has also been used to treat several noninfectious inflammatory skin diseases. However, the mechanisms underlying the improvement in such skin diseases remain unknown, and KI is not used widely. Thus, although KI is an old drug, physicians may not prescribe it frequently because they lack knowledge about it. While KI is very inexpensive and causes few side effects, it has been superseded by new powerful and expensive drugs, such as biological agents. It has been extensively studied in several mouse models how chronic, in particular chronic psychosocial, stressors facilitate the (re)activity of the innate immune system and, consequently, drive stress-associated pathologies. Here we first summarize the resulting concept and underlying mechanisms, proposing that social stress-induced bone marrow myelopoiesis, priming, emigration and activation of newly formed myeloid cells and accumulation of these cells in the spleen, gut, brain and fracture hematoma promote septic shock, colitis, anxiety and disturbed fracture healing, respectively. We further propose and discuss the hypothesis that it is not the social character of a particular stressor that promotes splenic invasion and subsequent full activation of stress-induced myeloid cells, but rather the occurrence of bite wounds as a result of direct physical interaction. Finally, we discuss the hypothesis that it is the combination of chronic stress, regardless of whether social or non-social in nature, and any kind of planned (i.e. surgery) or unplanned (i.e. [https://www.selleckchem.com/products/tepp-46.html ML265 price] bite wounds, injury) wounding that drives splenic invasion and subsequent full activation of stress-induced myeloid cells. BACKGROUND Signet Ring Cell adenocarcinoma (SRC) is a less common histological variant of esophageal adenocarcinoma (ACA). The low frequency of SRC limits the ability to make data-driven clinical recommendations for these patients. METHODS The National Cancer Database (NCDB) was queried for adult patients with clinical stage I, II or III adenocarcinoma of the non-cervical esophagus diagnosed between 2004-2015, stratified by SRC versus all other ACA variants. Cox proportional hazard regression models were adjusted for patient, tumor, and treatment characteristics. The role of surgery in SRC was evaluated among patients treated with chemoradiation alone versus chemoradiation with esophagectomy. RESULTS Of the 681 SRC and 13,543 ACA patients that underwent esophagectomy, no significant differences in age, sex, race or comorbidities were identified. Patients with SRC were more likely to have high-grade tumors (84% vs 41%, p less then 0.0001) and stage III tumors (47% vs 39%, p less then 0.0001) compared to ACA. Complete (R0) resection was less common in SRC (81% vs 90%, p less then 0.0001). Adjusted five-year mortality risk from surgery was higher for SRC patients compared to ACA (HR 1.24, 95% CI 1.13-1.37, p less then 0.0001). Among SRC tumors, chemoradiation with esophagectomy was associated with superior survival (HR 0.43, 95% CI 0.34-0.55, p less then 0.0001) compared to chemoradiation alone. CONCLUSIONS Among surgically-managed patients, SRC appears to have a worse prognosis than ACA, which may reflect the tendency of SRC tumors to be higher grade and more locally-advanced. However, SRC histology does not appear to diminish the role of esophagectomy in the management of locoregionally-confined esophageal cancer. INTRODUCTION AND AIM Real-word data on the head-to-head comparisons among glucagon-like peptide-1 receptor agonists (GLP-1RA) are scant. Therefore, we aimed to compare the effectiveness of dulaglutide versus liraglutide and exenatide once weekly (exeOW) in type 2 diabetic (T2D) patients under routine care. METHODS This was a retrospective, multicenter, real-world study on patients with T2D (aged 18-80) initiating a GLP-1RA between 2010 and 2018 at specialist outpatient clinics. We compared the effectiveness of dulaglutide versus liraglutide and exeOW on the changes in HbA1c (primary outcome), body weight, blood pressure and fasting glucose (secondary outcomes). Average follow-up was 5.9 months. Channelling biases were addressed with propensity score matching or multivariable adjustment. Meta-analyses of observational studies, covering the same comparisons, are also presented. RESULTS 849, 1371 and 198 patients were included in the dulaglutide, liraglutide and exeOW groups, respectively. The reduction of HbA1c was greater with dulaglutide than with liraglutide (-0.24 ± 0.08%; p = .003), and was confirmed in the meta-analysis of observational studies. In our study, dulaglutide showed similar effectiveness compared to exeOW. When these results were pooled with other observational studies, dulaglutide showed a greater reduction of HbA1c (-0.19%; p = .003) and body weight (-0.8 kg; p = .007). CONCLUSIONS In a real-world scenario, dulaglutide reduced HbA1c more than liraglutide. Conversely, we found similar effect of dulaglutide and exeOW, with statistical differences arising solely when results were meta-analysed with those from other observational studies. Lack of up-titration for liraglutide and higher discontinuation rate for exeOW likely influenced the estimated treatment difference. Among the most devastating sequelae of spinal cord injury (SCI) are genitourinary and gastrointestinal dysfunctions. Post-ganglionic neurons in pelvic ganglia (PG) directly innervate and regulate the function of the lower urinary tract (LUT), bowel, and sexual organs. A better understanding of how SCI affects PG neurons is essential to develop therapeutic strategies for devastating gastrointestinal and genitourinary complications ensuing after injury. To evaluate the impact of SCI on the morphology of PG neurons, we used a well- characterized rat model of upper thoracic SCI (T3 transection) that causes severe autonomic dysfunction. Using immunohistochemistry for neuronal markers, the neuronal profile size frequency distribution was quantified at one-, four-, and eight-weeks post SCI using recursive translation. Our investigation revealed an SCI-dependent leftward shift in neuronal size (i.e. atrophy), observable as early as one-week post injury. However, this effect was more pronounced at four and eight-weeks post-SCI.