The Privacy Limits of Transacting in Bitcoin

The Bitcoin blockchain, a prime example of disruptive technology, has fundamentally altered the way various industries approach remote transactions. Bitcoin grants privacy to its users by anonymizing public keys, provides autonomy by eliminating the need for trusted third parties, and maintains transparency through its public disclosure protocol. Bitcoin is an innovative manifestation of the Fourth Amendment ideals of security and autonomy. It is, thus, no surprise that the Bitcoin blockchain presents unprecedented Fourth Amendment challenges for courts to consider. In United States v. Gratkowski, the Fifth Circuit addressed the novel issue of whether Fourth Amendment protections extend to an individual’s Bitcoin transactions. Notably, the court was the first to find that an individual does not have a privacy interest in their information located directly on the Bitcoin blockchain. However, the Fifth Circuit applied inconsistent and flawed reasoning in reaching this decision, demonstrating a fundamental misunderstanding of Bitcoin and its users. Accordingly, this Note argues that the Gratkowski decision should be applied narrowly and with caution, especially considering the Supreme Court’s warnings against the incompatibility of current Fourth Amendment doctrine with the digital age. It then suggests implementing a modified reasonable expectation-of-privacy standard, supplementing the current standard with an additional inquiry into what information an individual disclosed when initiating a transaction. This modified standard would preserve the integrity of Bitcoin, while simultaneously articulating a proper framework for assessing privacy concerns in the context of Bitcoin and blockchain technology

Nausea and vomiting as major presenting symptoms of thyrotoxicosis after bilateral adrenalectomy for Cushing's disease

Thyrotoxicosis has a variety of presentations which depend on its severity and duration, as well as the age of the patient. In elderly patients, thyrotoxicosis may present with a variety of nonspecific symptoms. Nausea and vomiting as major presenting symptoms of thyrotoxicosis have rarely been reported. Thyrotoxicosis after adrenalectomy in patients with Cushing's syndrome and normal thyroid function, or with autoimmune thyroid dysfunction has rarely been reported previously. We describe a very rare case of an elderly patient with hypothyroidism due to Hashimoto's thyroiditis who presented with persistent nausea and vomiting as major presenting symptoms of thyrotoxicosis, which developed after bilateral adrenalectomy for Cushing's disease. Similar case has not been reported previously. In reporting this patient we aim at drawing attention to these forgotten symptoms of thyrotoxicosis, nausea and vomiting, and to emphasize that, at times, these symptoms may be the only presenting features of thyrotoxicosis, leading to considerable difficulty in diagnosis. Furthermore, cessation of glucocorticoid excess may sometimes be accompanied with thyrotoxicosis

Chronic Stanford type A aortic dissection manifesting as systemic inflammatory disorder

Typical presentation of type A aortic dissection usually encompasses severe acute chest pain, frequently radiating to the upper back, which is seen in more than 80% of the patients, while isolated back or abdominal pain have been repeatedly reported as the first manifestation of the disease as well. Occasionally, dyspnea due to acute aortic regurgitation, syncope, or stroke, secondary to obstruction of major cerebral vessels, have also been described at presentation of type A aortic dissection. Presentation of aortic dissection as a prolonged systemic illness with a number of nonspecific clinical and laboratory findings, such as low-grade fever, fatigue, malaise, weight loss, anemia, elevated acute phase response laboratory parameters, and absence of any of typical clinical features of the dissection syndrome has been only rarely reported. We describe a patient with type A chronic aortic dissection, manifesting as a systemic inflammatory disorder in the absence of acute chest syndrome. The diagnosis was made accidentally by computed tomography, ordered in the course of the regular work up. The patient underwent emergent surgery with resection and grafting of the dissected aorta. Pathological investigation demonstrated intense acute inflammation with neutrophilic infiltration in the vicinity of the intramural hemorrhage and necrosis, as well as granulation tissue with new vessels formation and collagen deposition in the outer media. The possible pathogenic mechanisms of the phenomenon are discussed

PrtT-Regulated Proteins Secreted by Aspergillus fumigatus Activate MAPK Signaling in Exposed A549 Lung Cells Leading to Necrotic Cell Death

Aspergillus fumigatus is the most commonly encountered mold pathogen of humans, predominantly infecting the respiratory system. Colonization and penetration of the lung alveolar epithelium is a key but poorly understood step in the infection process. This study focused on identifying the transcriptional and cell-signaling responses activated in A549 alveolar carcinoma cells incubated in the presence of A. fumigatus wild-type and ΔPrtT protease-deficient germinating conidia and culture filtrates (CF). Microarray analysis of exposed A549 cells identified distinct classes of genes whose expression is altered in the presence of germinating conidia and CF and suggested the involvement of both NFkB and MAPK signaling pathways in mediating the cellular response. Phosphoprotein analysis of A549 cells confirmed that JNK and ERK1/2 are phosphorylated in response to CF from wild-type A. fumigatus and not phosphorylated in response to CF from the ΔPrtT protease-deficient strain. Inhibition of JNK or ERK1/2 kinase activity substantially decreased CF-induced cell damage, including cell peeling, actin-cytoskeleton damage, and reduction in metabolic activity and necrotic death. These results suggest that inhibition of MAPK-mediated host responses to treatment with A. fumigatus CF decreases cellular damage, a finding with possible clinical implications

Role of C-Reactive Protein in Discrimination between Transudative and Exudative Pleural Effusions

Background: There is still no wide agreement regarding the efficacy of the serum levels of C-reactive protein (CRPs), pleural fluid levels of CRP (CRPpf), and their ratio (CRPr) in the discrimination between transudative (Tr) and exudative (Ex) pleural effusions (PEs). Most of the previous studies were conducted on small cohorts, and the role of CRPs in the CRPpf gradient (CRPg) in this discrimination has not been previously reported. The present study aims to assess the diagnostic efficacy of CRPs, CRPpf, CRPg, and CRPr in the discrimination between TrPE and ExPE in a relatively large cohort of patients with PE. Methods: The study population included 492 patients with PE, 210 of them with TrPE and 282 with ExPE. The levels of CRPs and CRPpf were measured, and the CRPg and CRPr were calculated. The values are presented as mean ± SD. Results: The mean levels of CRPs, CRPpf, CRPg, and CRPr of the TrPEs were 11.3 ± 5.7 mg/L, 4.6 ± 2.8 mg/L, 6.7 ± 3.9 mg/L, and 0.40 ± 0.14, respectively, and for the ExPEs, they were 140.5 ± 112.8 mg/L, 52.8 ± 53.2 mg/L, 87.2 ± 72.4 mg/L, and 0.37 ± 0.15, respectively. The levels of CRPs, CRPpf, and CRPg were significantly higher in the ExPEs than in the TrPEs (p < 0.0001). No significant difference was found between the two groups for the levels of CRPr (p = 0.15). The best cut-off value calculated by the receiver operating characteristic (ROC) analysis for discriminating TrPE from ExPE was for CRPs, 20.5 mg/L with area under the curve (AUC) = 97% and p < 0.0001; for CRPpf, 9.9 mg/L with AUC = 95% and p < 0.0001; and for CRPg, 13.6 mg/L with AUC = 96% and p < 0.0001. Conclusion: CRPs, CRPpf, and CRPg are strong markers for discrimination between TrPE and ExPE, while CRPr has no role in this discrimination

Crohn’s Disease with Atypical Extra-Intestinal Manifestations Developing Under Treatment with Vedolizumab

Crohn’s disease is a chronic inflammatory bowel disease that can affect any part of the GI tract, which is frequently associated with extra-intestinal manifestations. Pulmonary parenchymal disease is very uncommon and usually considered to be debilitating and harder to diagnose. Pulmonary granulomas are rarely described in the literature as a complication of Crohn’s disease. Here, we present a patient with Crohn’s disease exacerbation who developed granulomatous lung disease under treatment with vedolizumab. Our case may add evidence to the emerging theory that gut-selective biologic agents could lead to upregulation of some pro-inflammatory factors leading to the evolution of pulmonary disease

Chronic Stanford type A aortic dissection manifesting as systemic inflammatory disorder

Typical presentation of type A aortic dissection usually encompasses severe acute chest pain, frequently radiating to the upper back, which is seen in more than 80% of the patients, while isolated back or abdominal pain have been repeatedly reported as the first manifestation of the disease as well. Occasionally, dyspnea due to acute aortic regurgitation, syncope, or stroke, secondary to obstruction of major cerebral vessels, have also been described at presentation of type A aortic dissection. Presentation of aortic dissection as a prolonged systemic illness with a number of nonspecific clinical and laboratory findings, such as low-grade fever, fatigue, malaise, weight loss, anemia, elevated acute phase response laboratory parameters, and absence of any of typical clinical features of the dissection syndrome has been only rarely reported. We describe a patient with type A chronic aortic dissection, manifesting as a systemic inflammatory disorder in the absence of acute chest syndrome. The diagnosis was made accidentally by computed tomography, ordered in the course of the regular work up. The patient underwent emergent surgery with resection and grafting of the dissected aorta. Pathological investigation demonstrated intense acute inflammation with neutrophilic infiltration in the vicinity of the intramural hemorrhage and necrosis, as well as granulation tissue with new vessels formation and collagen deposition in the outer media. The possible pathogenic mechanisms of the phenomenon are discussed