Spleen-preserving distal pancreatectomy from multi-port to reduced-port surgery approach.

BACKGROUND: Minimally invasive pancreatic surgery via the multi-port approach has become a primary surgical method for distal pancreatectomy (DP) due to its advantages of lower wound pain and superior cosmetic results. Some studies have applied reduced-port techniques for DP in an attempt to enhance cosmetic outcomes due to the minimally invasive effects. Numerous recent review studies have compared multi-port laparoscopic DP (LDP) and multi-port robotic DP (RDP); most of these studies concluded multi-port RDP is more beneficial than multi-port LDP for spleen preservation. However, there have been no comprehensive reviews of the value of reduced-port LDP and reduced-port RDP. AIM: To search for and review the studies on spleen preservation and the clinical outcomes of minimally invasive DP that compared reduced-port DP surgery with multi-port DP surgery. METHODS: The PubMed medical database was searched for articles published between 2013 and 2022. The search terms were implemented using the following Boolean search algorithm: ("distal pancreatectomy" OR "left pancreatectomy" OR "peripheral pancreatic resection") AND ("reduced-port" OR "single-site" OR "single-port" OR "dual-incision" OR "single-incision") AND ("spleen-preserving" OR "spleen preservation" OR "splenic preservation"). A literature review was conducted to identify studies that compared the perioperative outcomes of reduced-port LDP and reduced-port RDP. RESULTS: Fifteen articles published in the period from 2013 to 2022 were retrieved using three groups of search terms. Two studies were added after manually searching the related papers. Finally, 10 papers were selected after removing case reports (n = 3), non-English language papers (n = 1), technique papers (n = 1), reviews (n = 1), and animal studies (n = 1). The common items were defined as items reported in more than five papers, and data on these common items were extracted from all papers. The ten studies included a total of 337 patients (females/males: 231/106) who underwent DP. In total, 166 patients (females/males, 106/60) received multi-port LDP, 126 (females/males, 90/36) received reduced-port LDP, and 45 (females/males, 35/10) received reduced-port RDP. CONCLUSION: Reduced-port RDP leads to a lower intraoperative blood loss, a lower postoperative pancreatic fistula rate, and shorter hospital stay and follow-up duration, but has a lower spleen preservation rate.

Reduced-port robotic pancreaticoduodenectomy versus open pancreaticoduodenectomy: a single-surgeon experience.

BACKGROUND AND OBJECTIVES: Multiple-port robotic pancreaticoduodenectomy (RPD) has been increasingly used as an alternative to open pancreaticoduodenectomy (OPD) in pancreatic cancer. However, the comparative safety and efficacy of reduced-port RPD versus OPD are unknown. METHODS: This was a prospective cohort study comprising adult patients who underwent reduced-port RPD (single-port or single-site plus one port) or OPD for malignant tumors of the pancreas and periampullary region from July 2015 to October 2020 at a single center. We collected data on the patient demographics, perioperative results, oncologic outcomes, and one-year survival. RESULTS: Forty-five patients underwent reduced-port RPD, and 13 underwent OPD. There were no significant differences in the age, sex, body mass index, ASA score, tumor location, or occurrences of postoperative complications between the two groups. Compared with OPD, reduced-port RPD was associated with less blood loss (300 ml [95% confidence interval {CI} 155-700] vs. 650 ml [95% CI 300-850], p value = 0.11) but a longer operative time (325 min [95% CI 290-370] vs. 215 min [95% CI 180-270], p value < 0.001). Compared with patients who underwent OPD, patients who underwent reduced-port RPD had a higher 1-year survival rate (68% [95% CI 49-81] vs. 22% [95% CI 3-51], log-rank, p value = 0.007). CONCLUSIONS: Reduced-port RPD can be safely performed in experienced surgeons and is associated with better perioperative and oncologic outcomes than OPD.

Generalized Frequency Division Multiplexing-Based Low-Power Underwater Acoustic Image Transceiver.

In this paper, a low-power underwater acoustic (UWA) image transceiver based on generalized frequency division multiplexing (GFDM) modulation for underwater communication is proposed. The proposed transceiver integrates a low-density parity-check code error protection scheme, adaptive 4-quadrature amplitude modulation (QAM) and 16-QAM strategies, GFDM modulation, and a power assignment mechanism in an UWA image communication environment. The transmission bit error rates (BERs), the peak signal-to-noise ratios (PSNRs) of the received underwater images, and the power-saving ratio (PSR) of the proposed transceiver obtained using 4-QAM and 16-QAM, with perfect channel estimation, and channel estimation errors (CEEs) of 5%, 10%, and 20% were simulated. The PSNR of the received underwater image is 44.46 dB when using 4-QAM with a CEE of 10%. In contrast, PSNR is 48.79 dB when using 16-QAM with a CEE of 10%. When BER is 10-4, the received UW images have high PSNR values and high resolutions, indicating that the proposed transceiver is suitable for underwater image sensor signal transmission.

Application of a commercial single-port device for robotic single-incision distal pancreatectomy: initial experience.

PURPOSE: Laparoscopic distal pancreatectomy has proven to be feasible and safe. Moreover, robotic surgery provides unique advantages for pancreatic procedures, although single-incision robotic pancreatic surgery is rarely discussed. We applied the single-port modified platform to accomplish robotic distal pancreatectomy in a series of patients. METHODS: The subjects of this study were ten patients who underwent robotic distal pancreatectomy in our hospital between July 1, 2015 and Dec 31, 2016. All patients were placed supine in the reverse Trendelenburg position with the legs abducted. Surgery was performed via a trans-umbilical 5.0-cm incision, using a modified single-port platform (LAGIPORT®) combined with the da Vinci Si Surgical System. The three arms and scope (30-degree up) were inserted through the LAGIPORT® and positioned in a triangle. Endoscopic ultrasound was used to localize the tumor and plan the resection margin. We recorded the surgical time, operation time, blood loss, postoperative pain score, hospital stay, and complications. RESULTS: The surgical time was 236 ± 32 min, the operation time was 172 ± 30 min, and the blood loss was 149 ± 65 ml. All patients underwent robot-assisted distal pancreatectomy without conversion. The average pain score on postoperative day (POD) 3 was 4.5 ± 1. Complications included subsplenic hematoma (n = 1) and minor pancreatic leakage (n = 2). There was no surgical mortality. CONCLUSIONS: Our results demonstrate the safety and efficiency of robotic single-incision distal pancreatectomy via the modified platform (LAGIPORT®).

Ubiquitin-specific protease 5 is required for the efficient repair of DNA double-strand breaks.

During the DNA damage response (DDR), ubiquitination plays an important role in the recruitment and regulation of repair proteins. However, little is known about elimination of the ubiquitination signal after repair is completed. Here we show that the ubiquitin-specific protease 5 (USP5), a deubiquitinating enzyme, is involved in the elimination of the ubiquitin signal from damaged sites and is required for efficient DNA double-strand break (DSB) repair. Depletion of USP5 sensitizes cells to DNA damaging agents, produces DSBs, causes delayed disappearance of γH2AX foci after Bleocin treatment, and influences DSB repair efficiency in the homologous recombination pathway but not in the non-homologous end joining pathway. USP5 co-localizes to DSBs induced by laser micro-irradiation in a RAD18-dependent manner. Importantly, polyubiquitin chains at sites of DNA damage remained for longer periods in USP5-depleted cells. Our results show that disassembly of polyubiquitin chains by USP5 at sites of damage is important for efficient DSB repair.

Novel method for site-specific induction of oxidative DNA damage reveals differences in recruitment of repair proteins to heterochromatin and euchromatin.

Reactive oxygen species (ROS)-induced DNA damage is repaired by the base excision repair pathway. However, the effect of chromatin structure on BER protein recruitment to DNA damage sites in living cells is poorly understood. To address this problem, we developed a method to specifically produce ROS-induced DNA damage by fusing KillerRed (KR), a light-stimulated ROS-inducer, to a tet-repressor (tetR-KR) or a transcription activator (TA-KR). TetR-KR or TA-KR, bound to a TRE cassette (∼ 90 kb) integrated at a defined genomic locus in U2OS cells, was used to induce ROS damage in hetero- or euchromatin, respectively. We found that DNA glycosylases were efficiently recruited to DNA damage in heterochromatin, as well as in euchromatin. PARP1 was recruited to DNA damage within condensed chromatin more efficiently than in active chromatin. In contrast, recruitment of FEN1 was highly enriched at sites of DNA damage within active chromatin in a PCNA- and transcription activation-dependent manner. These results indicate that oxidative DNA damage is differentially processed within hetero or euchromatin.

Damage response of XRCC1 at sites of DNA single strand breaks is regulated by phosphorylation and ubiquitylation after degradation of poly(ADP-ribose).

Single-strand breaks (SSBs) are the most common type of oxidative DNA damage and they are related to aging and many genetic diseases. The scaffold protein for repair of SSBs, XRCC1, accumulates at sites of poly(ADP-ribose) (pAR) synthesized by PARP, but it is retained at sites of SSBs after pAR degradation. How XRCC1 responds to SSBs after pAR degradation and how this affects repair progression are not well understood. We found that XRCC1 dissociates from pAR and is translocated to sites of SSBs dependent on its BRCTII domain and the function of PARG. In addition, phosphorylation of XRCC1 is also required for the proper dissociation kinetics of XRCC1 because (1) phosphorylation sites mutated in XRCC1 (X1 pm) cause retention of XRCC1 at sites of SSB for a longer time compared to wild type XRCC1; and (2) phosphorylation of XRCC1 is required for efficient polyubiquitylation of XRCC1. Interestingly, a mutant of XRCC1, LL360/361DD, which abolishes pAR binding, shows significant upregulation of ubiquitylation, indicating that pARylation of XRCC1 prevents the poly-ubiquitylation. We also found that the dynamics of the repair proteins DNA polymerase beta, PNK, APTX, PCNA and ligase I are regulated by domains of XRCC1. In summary, the dynamic damage response of XRCC1 is regulated in a manner that depends on modifications of polyADP-ribosylation, phosphorylation and ubiquitylation in live cells.