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Total esophagogastric dissociation
Published in Mark Davenport, James D. Geiger, Nigel J. Hall, Steven S. Rothenberg, Operative Pediatric Surgery, 2020
Riccardo Coletta, Antonino Morabito
The operation ends with the creation of a Stamm gastrostomy (Figure 29.7). Double purse-string sutures are placed on the body of the stomach. The opening will be at the level of the splenic hilum. A de Pezzer or Malecot catheter is introduced while the sutures are elevated. The stomach is secured to the abdominal wall and the catheter end is grasped from a counter-incision and the tube is brought out. A Heineke-Mikulicz pyloroplasty with 4/0 or 5/0 Maxon is only performed if there has been an accidental intraoperative injury to the vagus nerve or in the event of rescue TEGD. The abdominal wall is closed in layers with polyfilament absorbable suture (3/0 and 4/0 VicrylTM). The skin is approximated in BiosynTM 5/0 and skin glue.
Sphincter Repair in Crohn’s Disease
Published in Han C. Kuijpers, Colorectal Physiology: Fecal Incontinence, 2019
In textbooks about surgical technique the sphincter is usually depicted as a well-defined red muscle bundle. It is much different in reality, where it is difficult to distinguish the pale sphincteric tissue from the fibrous scar tissue. This distinction is important as one tries to save as much muscular tissue as possible. The epithelial mucosal layer is now repaired with Maxon* 000 or 0000. The rationale for using this type of material is to perform sutures with strong, nonreactive, monofilament, resorbable thread throughout the entire procedure. The only disadvantage is the very long delay required for degradation of the superficial sutures. Separate suturing of the internal and external sphincter is almost unfeasible, but care has to be taken to unite the sphincteric elements as close to the mucosa as possible in order to restore the internal sphincteric function. This is important to secure a good resting anal canal pressure. Although the overlap-technique of Parks is the standard procedure, it seems probable that in this way more ischemia is produced than with the apposition technique. A dilemma arises in so far as the muscle has to be dissected back to allow good approximation, while too extensive mobilization causes denervation and ischemia. The fatty subcutaneous tissue and the skin are closed with Maxon 000 or 0000. Suction drainage has been used, but healing by granulation of the partially open wound is preferred.
Hands
Published in Tor Wo Chiu, Stone’s Plastic Surgery Facts, 2018
The common choice is a non-absorbable monofilament (e.g. Prolene®, easier to use but in vitro tests have shown stretching under tension leading to a tendon gap) or non-absorbable braided (Ticron®, braided sutures have a tendency to cause deformation and need greater attention to detail in their placement and tightening). Absorbable sutures (PDS, Maxon®) are not commonly used but can also be satisfactory since the metabolic rate of the tendon tissue is low, and suture material is retained long enough to maintain tensile strength during healing.
The effect of horizontal forces from a Smart Walker on gait and perceived exertion
Published in Assistive Technology, 2022
Wen Liang Yeoh, Jeewon Choi, Ping Yeap Loh, Seiji Saito, Satoshi Muraki
The motors used were Maxon EC 45 flat brushless DC motors with integrated encoders and 15:1 planetary gearhead (Maxon Motor, Switzerland). The motors were controlled using a TMS320F28379D Launchpad microcontroller and two BOOSTXL-DRV8301 (Texas Instruments, USA) motor drivers. Power was supplied through a 24 V switched-mode power supply, the RWS600B-24 (TDK, Japan), connected to the mains using extension cables. Additionally, external braking resistors were connected parallel to the power supply and regulated using a MOSFET switch to dissipate the regenerative energy generated when braking.
Clonal evolution in a chronic neutrophilic leukemia patient
Published in Hematology, 2019
Qi-Guo Zhang, Jing Wang, Wen-Yu Gong, Qi-Chuan Jin
The current study, first, confirms the observations by Maxon et al. [1] regarding the association between CNL and CSF3R mutations. Second, it presents a complete picture of the mutational profiling of the pathogenesis of CNL, which is certainly more complex than expected from previous reports. Approximately 75% of patients with CNL who have CSF3R mutations exhibit only membrane-proximal mutations, whereas the other 25% of patients harbor both membrane-proximal and truncating-compound mutations [3]. The scarcity of truncation mutations alone in CNL raises the possibility that truncation mutations alone are insufficient to drive the malignancy and that cooperating mutations in CSF3R or other genes may be required [4]. The CSF3R truncation mutation is not sufficient for leukemia but represents an early event in leukemogenesis. Truncation mutations alone do not cause leukemia in mouse models [5], but they can accelerate the development of disease in the presence of another genetic event driving leukemia [6]. Consistent with the in vivo data, the CSF3R truncation mutations display slower cell transformation kinetics than the T618I mutation in cellular assays and require ligands for the activation of downstream signaling pathways [1,7], which reduces the differentiative capacity of the receptor while continuing to allow for cellular proliferation. In our case, truncation mutations in the SRSF2 and TET2 genes are sufficient to drive leukemogenesis in the CNL, and CSF3R membrane-proximal mutations occur as a secondary event within the context of clonal hematopoiesis. The process of clonal hematopoiesis is originally associated with somatically acquired variants in genes that regulate epigenetic (TET2) and splicing (SRSF2) processes. Acquisition of a CSF3R signaling mutation gives the clonal hematopoietic population a neutrophil lineage bias. Because patients with CNL who have only truncation mutations in CSF3R are apparently rare, it seems likely that the clone evolves to acquire additional mutations in epigenetic and splicing genes, which amplify the disease process. Interestingly, concomitant SRSF2 and TET2 mutations were not observed in any other CNL cases, though this was not statistically significant [8]. These mutations may provide a backdrop for a later-occurring CSF3R mutation, which, in turn, imparts a neutrophilic phenotype resulting in CNL.