Journal of Nippon Medical School = Nippon Ika Daigaku zasshi
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Sepsis is a devastating and complex syndrome and continues to be a major cause of morbidity and mortality among critically ill patients at the surgical intensive care unit setting in the United States. The occurrence of sepsis and septic shock has increased significantly over the past two decades. Despite of highly dedicated basic research and numerous clinical trials, remarkable progress has not been made in the development of novel and effective therapeutics. ⋯ In this regard, the role of inflammation in the pathophysiology of sepsis, although still incompletely understood, is clearly critical. Recent findings resulting from vigorous investigations have contributed to delineate various novel directions of sepsis therapeutics. Among these, this review article is focused on new promising mechanisms and concepts that could have a key role in anti-inflammatory strategies against sepsis, including 1) "inflammasome": a multiprotein complex that activates caspase-1; 2) "the cholinergic anti-inflammatory pathway": the efferent arm of the vagus nerve-mediated, brain-to-immune reflex; 3) "stem cells": unspecialized and undifferentiated precursor cells with the capacity for self-renewal and potential to change into cells of multiple lineages; 4) "milk fat globule-EGF factor VIII (MFG-E8)": a bridging molecule between apoptotic cells and phagocytes, which promotes phagocytosis of apoptotic cells.
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Radical prostatectomy (RP) for localized prostate cancer after transurethral resection of the prostate (TUR-P) is technically difficult because of periprostatic adhesion and changes in the form of the prostate. The advantages of laparoscopic RP (LRP) over retropubic RP (RRP) include a less invasive operation through a small wound, a clearer field of vision, and reduced blood loss, and, therefore, LRP may represent the optimal method for RP after TUR-P. The present study compared clinical, oncological, and pathological outcomes between LRP and RRP after TUR-P at our institution. ⋯ We found no significant differences in clinical, pathological, and oncological outcomes, except for urinary incontinence, between LRP and RRP.
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Case Reports
Two cases of flexor digitorum profundus avulsion due to enchondroma of the distal phalanx.
Avulsion of the flexor digitorum profundus tendon with fracture of the distal phalanx is rare. Moreover, enchondroma is less frequent in the distal phalanx. We report two unusual cases of avulsion of the flexor digitorum profundus tendon at its insertion in combination with pathological fracture of the distal phalanx due to enchondroma. ⋯ At the final follow-up examinations, there were no symptoms and no recurrence of the bone tumor. In the present cases, three-dimensional computed tomography imaging was useful for diagnosing the flexor tendon avulsion, determining the preoperative identification the location of a ruptured tendon stump, and planning the operation to minimize the surgical wound. The recommended treatment for avulsion of the FDP tendon due to enchondroma is curettage, bone grafting of the resultant cavity, and reattachment of the tendon to ensure sufficient structural strength to permit secure fixation and early mobilization and, especially, to prevent flexion contracture of the finger because the stump of the flexor digitorum profundus is buried in the cavity of the distal phalanx.
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We report 2 cases of ruptured aneurysms of the posterior inferior cerebellar artery associated with an arteriovenous malformation (AVM). The aneurysm and AVM were simultaneously embolized with n-butyl cyanoacrylate. ⋯ In both cases the aneurysms were successfully occluded. The effectiveness and limitations of this treatment are discussed.
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Myofibroblasts play a critical role in tissue fibrosis. However, the intracellular signaling pathways in myofibroblast differentiation are poorly understood. Here, we studied the relationship between transforming growth factor-β (TGF-β)/Smad pathway activation and myofibroblast differentiation in both in vivo and in vitro experiments. ⋯ However, TGF-β1 produced no effect on the quantity of ASMA, either in mRNA levels or protein levels, even after the phosphorylation of Smad2/3. In contrast, TGF-β1 upregulated the expression of type I collagen mRNA. These findings suggest that in pulmonary fibrosis the molecular mechanism of myofibroblast differentiation is complex and that the difference between ASMA expression and type I collagen expression is mediated by the TGF-β/Smad pathway.