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Lymphatic anatomy: lymphatics of the uterus
Published in Charles F. Levenback, Ate G.J. van der Zee, Robert L. Coleman, Clinical Lymphatic Mapping in Gynecologic Cancers, 2022
Jennifer J. Mueller, Nadeem R. Abu-Rustum
Lecuru et al. injected a colored dye into the uterus of 11 female cadavers, 5 within the corpus and 6 within the cervix, and mapped lymphatic drainage to determine any difference in these patterns for cervical versus uterine malignancies.5 The cervical injections drained primarily to internal iliac nodes, with no paraaortic connections. The corpus injections drained to nodes posterior to the external iliac vessels in the obturator region primarily and, less commonly, to the paraaortic region. In summary, uterine lymphatic drainage pathways consistently follow an ovarian drainage pathway to the aortic and gluteal nodal region, a round ligament drainage pathway to the inguinofemoral nodal region, and a cervical/midbody uterine drainage pathway to the external iliac and obturator nodal region, as well as the common, internal iliac, and presacral nodal region (Figure 5.1).
Picture Frame Sign
Published in Michael E. Mulligan, Classic Radiologic Signs, 2020
‘One picture is worth more than a thousand words’ says the Chinese proverb1. Picture frames can also be very expressive, as is the case with the term used for one type of Pagetoid change seen in a vertebral body. Georg Schmorl2,3 (1861–1932), who wrote extensively on disorders of the spine, gave radiologists this picture-frame analogy in two of his articles that dealt with Pagetoid changes in the spine. He correlated the gross pathologic and roentgenographic changes of Paget’s disease in the spinal column. Schmorl found that in Paget’s disease the trabeculae at the edges of the vertebral bodies seemed compacted and were more dense than those in the midbody. To him, these compact dense trabeculae surrounding the midbody suggested the likeness of a framework or picture frame (rahmenartig). This appearance of a coarsened thickened framework, outlining a vertebral body, is a roentgen classic that is diagnostic of Paget’s disease (Figures 1 and 2). No other words are necessary when one sees this ‘picture frame’.
Complications of Gastric Surgery
Published in Stephen M. Cohn, Matthew O. Dolich, Complications in Surgery and Trauma, 2014
Kevin M. Schuster, Erik Barquist
The mainstay of therapy for gastric cancer is surgery, which provides the only hope of cure. At the time of operation, if no gross metastases are found, a curative resection should be attempted. The goal is to completely remove the primary tumor and the associated lymph nodes. However, the extent of gastric resection required and the role of radical lymphadenectomy in achieving cure have been controversial. Margins of 4–6 cm around the primary tumor are required. For distal lesions, subtotal gastrectomy with a Billroth II anastomosis is the most frequently used procedure.1 Lesions of the midbody or the fundus require total gastrectomy. Other indications for total gastrectomy include gastric stump cancer after distal resection for benign disease, Linitus plastica, and cancer associated with multiple polyps. Reconstruction is usually through an end-to-side Roux-en-Y esophagojejunostomy. Lesions near the gastroesophageal junction require esophagogastrectomy. Proximally, at least 10 cm of esophagus should be resected, with frozen section to ensure adequate margins. Gastric cancer can now be resected by three distinct methods that include laparotomy, laparoscopy, and endoscopic methods. The latter two methods are primarily reserved for lower stage disease. There is less blood loss and fewer complications associated with a laparoscopic approach and similar long-term survival when compared to open methods.2,3 The types of complications are however similar.
DNA-dependent protein kinase: effect on DSB repair, G2/M checkpoint and mode of cell death in NSCLC cell lines
Published in International Journal of Radiation Biology, 2019
Ali Sak, Michael Groneberg, Martin Stuschke
However, the precise role of DNA-PKcs in determining the radiosensitivity of cells has not been elucidated. The DNA-PKcs has pleiotropic effects with (i) inhibition of NHEJ for DNA double-strand break repair (Sak et al. 2002), (ii) triggering DSB induced apoptosis (Abe et al. 2008), and (iii) activation of the G2 checkpoint in response to IR (Arlander et al. 2008). In addition, the localization of phosphorylated DNA-PKcs at centrosomes, kinetochores, and midbody implies that DNA-PKcs play a direct role in regulating mitotic progression (Shang et al. 2010) and may therefore have an effect on the stability of spindle formation (Shang et al. 2010). Yu et al. (2015) also clearly demonstrated the different mode of cell death activated by the cell lines upon pharmacological inhibition of DNA-PK with NU7441, depending on the genetic background of the cells. Although DNA-PK is well known for its function in the NHEJ pathway of DNA double-strand break repair, its involvement in mitotic progression after DNA damage provides an interesting prospect for understanding the mechanism coupling DNA repair, cell cycle progression and survival after irradiation. NHEJ, in contrast to HR, was shown to function at all stages of the cell cycle and does not require the presence of a homologous template and is therefore highly error prone. This proneness to errors can increase the risk for mutations and genetic instability. However, the risk of mutation as a result of DNA damage repair by NHEJ is balanced by activation of cell cycle arrest and thus of avoiding catastrophic cell division in the presence of DSBs.
Ultra-long silver nanowires induced mitotic abnormalities and cytokinetic failure in A549 cells
Published in Nanotoxicology, 2019
Fengbang Wang, Ying Chen, Yuanyuan Wang, Yongguang Yin, Guangbo Qu, Maoyong Song, Hailin Wang
We used long-term time-lapse video microscopy to analyze mitotic events in the A549 cell line. By using this system, we were able to track the fate of progeny from multipolar mitosis and of cells that subsequently underwent multipolar mitosis. Interestingly, we observed that two daughter cells often remerged into one giant cell during cytokinesis (Figure 5(c)), indicating cytokinesis failure and multipolarity induced by AgNW treatment. Aurora B is a kinase located at the midzone during telophase and at the flanking regions of the midbody during cytokinesis (Hu, Coughlin, and Mitchison 2012). The inactivation of Aurora B can cause cytokinesis to progress and abscission to occur, but the activation of Aurora B inhibits the late stages of cytokinesis (Carmena 2008; Agromayor and Martin-Serrano 2013). Here we presumed direct physical contact with ultra-long AgNWs as an involved mechanistic explanation for cytokinesis failure. During telophase, A549 cells entered into cytokinesis while cells remained interconnected by an intercellular bridge with a phase-dense midbody at the center. After AgNWs treatment for 12 h, AgNWs, particularly AgNW30, were often observed in the intercellular bridge between two daughter cells and promoted the accumulation of Aurora B in the midbody (Figure 5(d)). This result indicates that ultra-long AgNWs may obstruct the contractile ring and inhibit abscission of the cytokinetic furrow. Although whether AgNWs directly interact with the midbody was not confirmed, cells with chrysotile fibers in the intercellular bridge could finish cytokinesis, delivering the fiber to one of the cells after severing the bridge at one point (Cortez et al. 2016).
PLK4: a link between centriole biogenesis and cancer
Published in Expert Opinion on Therapeutic Targets, 2018
Radhika Radha Maniswami, Seema Prashanth, Archana Venkataramana Karanth, Sindhu Koushik, Hemalatha Govindaraj, Ramesh Mullangi, Sriram Rajagopal, Sooriya Kumar Jegatheesan
PLK4 exhibits differential localization in accordance to various stages of cell cycle. The sequences upstream of the C-terminal polo box direct the correct localization of PLK4 [61]. Experiment conducted in mouse fibroblasts revealed the localization of PLK4 to the nucleolus and centrosome during the G2 and early M phase, respectively. PLK4 localization is scattered throughout the cell during anaphase, while is constrained to the midbody cleavage furrow during telophase. Furthermore, perinuclear localization was observed during interphase [42].