Purpose: Splenic flexure mobilization (SFM) is occasionally utilized during sigmoidectomy to facilitate a tension-free colorectal anastomosis. Present literature regarding its use, safety, and efficacy predominantly evaluates traditional laparoscopic vs. open techniques, thus not adequately representing the current minimally invasive surgical landscape. Methods: This retrospective cohort analysis evaluated SFM during sigmoidectomy for diverticular disease via traditional laparoscopic, single-incision laparoscopic, and robotic techniques at a United States academic institution from 2019 to 2022. Primary outcomes were the rate of SFM, independent predictors, and short-term outcomes. Results: A total of 117 patients underwent sigmoidectomy for diverticulitis by six colorectal surgeons, of whom 27 underwent SFM. SFM was associated with higher rates of complicated diverticulitis (85.2% vs. 46.7%, p < 0.001), including abscess (55.6% vs. 33.3%, p = 0.037) and fistulae (59.3% vs. 17.8%, p < 0.001). Presence of a fistula was an independent predictor of SFM by logistic regression (odds ratio [OR], 5.886; p < 0.001). Mobilization was associated with more concomitant surgical procedures (66.7% vs. 28.9%, p < 0.001). There was a significant association between SFM and conversion to open approach (14.8% vs. 3.3%, p = 0.049), longer length of stay (4.2 ± 2.8 days vs. 3.6 ± 4.3 days, p = 0.041), and increased operative time (241.7 ± 76.4 minutes vs. 199.2 ± 75.7 minutes). There was no difference in 30-day morbidity/mortality. Conclusion Routine SFM can be considered in minimally invasive sigmoidectomy for complicated diverticulitis without significant impact on 30-day morbidity/mortality regardless of surgical approach and may be anticipated preoperatively, particularly when a fistula is present.

멘델 무작위화(Mendelian randomization, MR) 연구는 조절 가능한 노출(modifiable exposure)이 건강결과에 미치는 인과효과(causal effect)를 더 잘 이해하게 해 주지만, 그 근거는 종종 보고가 불충분함으로 인하여연구 결과의 해석과 적용에 한계가 있을 수 있다. 보고지침은 흔히 무슨 연구를 하고 무엇을 발견했는지 독자가 쉽게 이해하도록 돕는다. STROBE-MR(관찰연구의 멘델 무작위화를 활용한 보고지침)은 MR 연구를 명확하고 투명하게 보고하도록 돕는다. STROBE-MR을 논문 작성에 활용하면 독자, 심사자, 학술지 편집인이 MR 연구의 보고 품질과 완성도를 평가하는 데 도움이 될 것이다. 이 글은 STROBE-MR 체크리스트 20개 항목의 의미와 근거를 설명하고, 각 항목마다 사례를 제시해 독자가 잘 이해할 수 있는 논문 작성법을 설명하려고 하였다.

Results: Propensity matching led to two groups of 89 patients each. The UIV, pelvic incidence minus lumbar lordosis, sagittal vertical axis, pelvic tilt, age, and body mass index were similar in both groups (p >0.05). The incidence of PJK at postoperative one year was similar for SE (30.3%) and LF (22.5%) groups (p =0.207). The PJK angle was comparable (p =0.963) with a change of −8.2° (SE) and −8.3° (LF) from the preoperative measures (p =0.954). A higher rate of PJK after SE (p =0.026) was found only in the subgroup of patients with UIV levels between T9 and T12. Conclusions Instrumentation to the sacrum with or without iliac extension did not increase the overall risk of PJK. However, an increased risk for PJK was found after SE with UIV levels between T9 and T12.

There is evidence that a substantial part of genetic predisposition to prostate cancer (PCa) may be due to lower penetrance genes which are found by genome-wide association studies. We have recently conducted such a study and seven new regions of the genome linked to PCa risk have been identified. Three of these loci contain candidate susceptibility genes: MSMB, LMTK2 and KLK2/3. The MSMB and KLK2/3 genes may be useful for PCa screening, and the LMTK2 gene might provide a potential therapeutic target. Together with results from other groups, there are now 23 germline genetic variants which have been reported. These results have the potential to be developed into a genetic test. However, we consider that marketing of tests to the public is premature, as PCa risk can not be evaluated fully at this stage and the appropriate screening protocols need to be developed. Follow-up validation studies, as well as studies to explore the psychological implications of genetic profile testing, will be vital prior to roll out into healthcare.
Genetic Predisposition to Disease ; genetics ; Genetic Testing ; Humans ; Kallikreins ; genetics ; Male ; Membrane Proteins ; genetics ; Prostatic Neoplasms ; diagnosis ; genetics ; Prostatic Secretory Proteins ; genetics ; Protein-Serine-Threonine Kinases ; genetics ; Risk Factors

Suppressor of cytokine sigaling (SOCS) genes encode a family of protein recently identified as negative feedback inhibitors of signaling by eytokine receptors. We have previously shown that endotoxin markedly stimulates SOCS gene expression in rat liver, that correlates with observed resistance to growth hormone-signaling during endotoxemia. The objective of this study was to determine the expression of SOCS genes in state of fasting that have been shown to cause altered responses in pro-inflammatory cytokines and anzbolic hormones. Male Sprague-Dawley rats (～200g) were fasted for 1, 2 or 3 days, or refed for 3 days following a 3-day period of fasting. Liver and muscle mRNAs were determinedby Northern blotting using specific rat cDNA probes cloned in our laboratory. In liver, after a l-day lag period, there was a progressive 2-fold increase in SOCS-3 and 75% decrease in SOCS-2 mRNA afte 2 and 3 of fasting. Both SOCS mRNAs were normalized by 3 days of refeeding. There was no measurable changes in tyrosine phosphorylation of STAT1, STAT3, STAT5a or STAT5b, nor activation of MAP kinases including ERK 1/2, p38, and JUNK 1/2 in liver by 3 days of fasting. In muscle, there was a similar 75% decrease in SOCS-2 mRNA, but no change in SOCS-3 mRNA following 3 days of fasting. These data suggest that malnutrition regulates SOCS-2 and SOCS-3 in a different way, and this regulation is tissue specific. The changes of SOCS mRANs are independent of measurable phosphoryiation of multiple STATs and activation of MAP kinasea. The altered SOCS expressions during fasting may explain the changes of biological effects of multiple cytokines and anabolie hormones in malnutrition states.

No abstract available.
Germ Cells* ; Humans ; Neoplasms, Germ Cell and Embryonal* ; Treatment Outcome* ; Biomarkers, Tumor*