A Case of Metastatic Chromophobe Renal Cell Carcinoma Masked as Suspected Hepatic Abscesses.

Background: Characterizing multiple hepatic lesions on cross-sectional imaging, particularly differentiating abscesses from metastatic lesions, can be challenging. Case Presentation: A male aged 53 years with a history of chromophobe renal cell carcinoma presented with fevers and abdominal pain and was found to have multiple hepatic lesions concerning for hepatic abscesses. The lesions initially evaded diagnosis on imaging, laboratory tests, and biopsy, but ultimately were determined to be a rare case of metastatic chromophobe renal cell carcinoma of the liver. Conclusions: The finding of multiple new liver lesions on imaging during a febrile illness is concerning for hepatic abscess or malignancy, which can be difficult to diagnose with imaging alone. Differentiation between infectious and neoplastic etiologies may require additional imaging and/or tissue sampling.

Bleeding Gastrointestinal Stromal Tumor (GIST) Results in a Sticky Situation: The Good and Bad of Hemostatic Spray.

A 50-year-old female presented with symptomatic anemia and hematemesis due to a 3.3 cm gastric gastrointestinal stromal tumor (GIST), which was located in the fundus. Adequate endoscopic views were only achieved in the retroflexed position and attempts at hemostasis via endoscopic clips were unsuccessful. Subsequently, TC-325 hemostatic powder was sprayed on the bleeding lesion and given retroflexed positioning, the powder also coated the esophagogastroduodenoscopy (EGD) scope where it abutted the gastroesophageal junction (GEJ). Hemostasis was successful, but the scope was unable to be withdrawn due to adherence to the surrounding mucosa. With torque maneuvering and a moderate amount of withdrawal force, the scope was successfully freed. The patient was started on imatinib mesylate and did not experience further bleeding episodes. This case highlights the challenge of achieving hemostasis in a bleeding GIST, the beneficial role of hemostatic powder spray, and the need for caution when utilizing it in a retroflexed manner.

Desipramine induced changes in the norepinephrine transporter, alpha- and gamma-synuclein in the hippocampus, amygdala and striatum.

The high incidence of depression in Parkinson's disease (PD) has been well documented in the clinic; however, the underlying molecular mechanisms of these overlapping pathologies remain elusive. Using a rodent model of depression, the Wistar-Kyoto (WKY) rat, we previously demonstrated that in the frontal cortex the altered expression and protein interactions of alpha- and gamma-synuclein (alpha-Syn, gamma-Syn) were associated with dysregulated trafficking of the norepinephrine transporter (NET). Chronic treatment with desipramine (DMI), a NET-selective antidepressant, caused a disappearance of depressive-like behavior that was accompanied by a change in alpha-Syn and gamma-Syn expression and their trafficking of NET. Using this same model, we examined the expression of NET, alpha-Syn and gamma-Syn in the hippocampus, amygdale, brainstem, and striatum, all regions implicated in the development or maintenance of depression or PD pathology. Following chronic treatment with DMI, we observed a significant decrease in NET in the hippocampus, amygdala, and brainstem; decrease in gamma-Syn in the hippocampus and amygdala; and, increase in alpha-Syn in the hippocampus and amygdala. Unexpectedly, we observed a significant decrease in alpha-Syn expression in the striatum of the WKY following chronic DMI treatment. The altered expression of NET, alpha-Syn and gamma-Syn in different brain suggest that DMI's ability to improve depressive-like behavior in a rodent is associated with region-specific changes in the regulation of NET by alpha- and gamma-Syn.

Desipramine modulation of alpha-, gamma-synuclein, and the norepinephrine transporter in an animal model of depression.

The mechanisms underlying depression remain elusive. We previously determined that alpha-synuclein (alpha-Syn) modulates the activity and trafficking of the norepinephrine transporter (NET) in a manner that is dependent on its interactions with microtubules (MTs). Here we sought to determine if alpha-Syn, or the other synuclein family members, beta-synuclein (beta-Syn) and gamma-synuclein (gamma-Syn), modulate NET activity in an animal model of depression, the Wistar-Kyoto (WKY) rat. The NET-selective antidepressant desipramine (DMI) was chronically administered for 14 days to WKY rats and the strain from which it was outbred that does not show depressive-like behavior, the Wistar rat. This drug regimen induced significant behavioral improvements in the WKY, but not the Wistar rat, in the forced swim test. In WKY rats there was an overexpression of gamma-Syn which was reduced following DMI treatment. In parallel, DMI caused an increase in both alpha-Syn and NET in the frontal cortex. Frontal cortex synaptosomes from WKY rats were not sensitive to nocodazole, a compound that promotes MT destabilization. However, in WKYs treated with DMI, nocodazole induced an increase in [(3)H]-NE uptake. This trend was reversed in Wistars. Underlying these DMI-induced changes were alterations in the protein interactions between the synucleins and NET with the tubulins. These results are the first to implicate alpha-Syn or gamma-Syn in the pathophysiology of depression and suggest that targeting synucleins may provide a new therapeutic option for depression.