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The Injured Cell
Published in Jeremy R. Jass, Understanding Pathology, 2020
Liquefactive necrosis occurs when there is rapid dissolution of cells. This is the usual outcome of necrosis in the brain that is of ischaemic origin. Formation of an abscess may also be described as liquefactive necrosis. Fat necrosis affects adipose tissue and is a typical feature associated with acute inflammation of the pancreas (pancreatitis). The enzyme lipase released by the injured pancreas converts triglycerides into free fatty acids. These are in turn converted to calcium soaps which appear macroscopically as white chalky areas and histologically as amorphous blue deposits. The fourth type of necrosis is caseous necrosis, associated typically with tuberculosis. The necrotic tissue has a soft, dry and cheese-like consistency.
The histotripsy spectrum: differences and similarities in techniques and instrumentation
Published in International Journal of Hyperthermia, 2023
Randall P. Williams, Julianna C. Simon, Vera A. Khokhlova, Oleg A. Sapozhnikov, Tatiana D. Khokhlova
In comparing shock-scattering and intrinsic threshold histotripsy in fibrous tissues, per a recently reported study in resected human uterine leiomyomas, shock-scattering histotripsy with 5-cycle pulse duration only achieved the formation of scattered areas of disruption within targeted tissue, similarly to BPH [116]. Intrinsic threshold histotripsy exposures resulted in a more defined (i.e., less diffuse) bubble cloud, as per US imaging, and achieved full fractionation, albeit only at a very large treatment time, more than 100 times over that required for soft tissue ablation. It should be noted, however, that the 5-cycle pulses were delivered at higher PRF compared to single-cycle pulses, which may have confounded the comparison. Another interesting aspect of this study was the presence of coagulative necrosis, along with liquefactive necrosis in all successful exposures, further supporting the concept of using heat to enhance fractionation.
An unusual and delayed complication of hyaluronic acid filler injection: a case report
Published in Case Reports in Plastic Surgery and Hand Surgery, 2020
Narges Horriat, Tina R. Woods, Abelardo Medina
Upon admission, patient exhibited verrucous granuloma-like skin lesions on glabellar region, nasolabial folds and marionette lines (Figure 2(A,B)). CT face scan with IV contrast revealed abnormal cutaneous and subcutaneous heterogeneous enhancing consistent with phlegmon or early abscess formation (Figure 2(C,D)). She was treated with amphotericin B (5 mg/kg IV q24h for 2 weeks) guided by infectious disease consultants. In addition, local cultures of the lesions reported the presence of Eschericia coli, Enterococcus faecalis, and Staphylococcus epidermidis. Accordingly, vancomycin (15 mg/kg IV q12h) and meropenem (2 g IV q8h) were also added for 1 week. On post-admission day 15, we proceeded with definitive surgical debridement via wide local excision followed by wound care for healing by secondary intention (Figure 3(A–D)). On gross examination, the specimens appeared granulomatous in nature with liquefactive necrosis (Figure 4(A)). Final pathology reported the presence of squamous epithelium with chronic lymphohistiocytic inflammation and fibrinopurulent exudate including foreign body giant cells (Figure 4(B)). Grocott’s methenamine silver (GMS) stain with adequate positive and negative controls were negative for fungal infection.
Sevoflurane reduces ischemic brain injury in rats with diet and streptozotocin-induced diabetes
Published in Journal of Receptors and Signal Transduction, 2018
Huapeng Zhang, Huayong Chen, Wei Wang, Baoze Zhang, Lingzhi Yu
In the study, we mainly discussed the ischemia stroke. The hypoxia caused by ischemic stroke will impairs oxidative phosphorylation and reduces ATP production in neuronal tissue [11]. The initial phase of injury shows a hallmark of cellular swelling which causes microvilli and membrane blebbing, ribosome dissociation, and malfunction of protein synthesis [12]. This process is reversible but will become irreversible damage if not effectively treated [12]. The hallmark for irreversible damage is membrane damage [13]. The irreversible cellular damages lead to apoptosis, necrosis, and neuronal loss eventually [14]. Apoptosis is initiated by inactivation of Bcl-2 and activation of Bax due to cellular injuries [15]. This further leads to cytochrome c release, caspase activation, and subsequent apoptosis. For necrosis, acute inflammation and other pathological changes will cause liquefactive necrosis in brain [16]. Oxidative stress, genes like eNOS S1176 phosphorylation site, signaling pathways play a critical role in the process of pathogenesis of diabetic stroke [17,18]. Hence, oxidative stress and neuron apoptosis after ischemia are the major pathways that drive neuronal cell death and whether they are implicated in ischemic process needs to be illuminated.