Ureter Injury in Laparoscopic Para-Aortic Lymphadenectomy for Endometrial Cancer by the Transperitoneal Approach.

The patient was 66 years old, had three pregnancies and two deliveries, and was menopausal at the age of 51. She had irregular bleeding and was found to have a chicken-egg-sized uterus and a thickened endometrium (23 mm). She underwent laparoscopic surgery for uterine endometrial cancer (endometrioid carcinoma G1, stage IB). Laparoscopic simple hysterectomy, bilateral adnexectomy, pelvic lymph node dissection, para-aortic lymph node dissection, and partial omentectomy were performed using the transperitoneal approach (TPA). The patient was obese, with a height of 148 cm, a weight of 68 kg, and a body mass index of 31 kg/m2. She had a large amount of visceral fat, which made it difficult to expand the surgical field during para-aortic lymph node dissection. A laparoscopic fan retractor (EndoRetract II, Medtronic) was used to lift the intestinal tracts and expand the field of view. It broke the fat around the left kidney, and the exposed left ureter was heat-damaged using a vessel sealing device (LigaSure, Medtronic). Postoperatively, a left ureteral stent was placed, and continuous urine draining into the retroperitoneum was performed. To prevent injury to the left ureter, the left ovarian vein branching from the left renal vein should be exposed as a landmark before the left ureter running parallel to it is isolated. It is essential that the fat around the left kidney is not broken during this operation. The left iliopsoas muscle should be exposed, and using this as a base, the left ovarian vein, left ureter, and left perirenal fat should be compressed and moved to the left side using a fan retractor to ensure a safe operation.

Ureter Injury in Total Laparoscopic Hysterectomy.

Objective: To identify surgical manipulations that caused ureter injury during total laparoscopic hysterectomy (TLH) and evaluate the surgical manipulations to identify ways to prevent such injury. Patients and Methods. This single-center, cross-sectional study included 1135 cases of TLH performed for benign diseases from January 2009 to December 2021. Seven cases (0.6%) that needed ureteral stent placement intra- or postoperatively for ureter injury were included. We identified the surgical manipulations that caused ureter injury from surgical videos. Results: Two cases had adhesions around the bladder pillar, and the ureter sustained a thermal injury during the cardinal ligament transection. One case had severe endometriosis, and the ureter was bluntly damaged when the adhesion was released. In one case, the ureter was thermally damaged during bipolar hemostasis for uterine artery bleeding. In two cases, the obliterated umbilical artery was mistaken for the ureter, and the real ureter was injured. In one case, ureteral peristalsis was inhibited by a pelvic abscess caused by postoperative infection. Conclusion: To prevent ureter injury during TLH, the ureter should be isolated in case of severe adhesion. Moreover, the following could be considered: (1) expand Okabayashi's pararectal space lateral to the uterosacral ligament, (2) perform dissection sharply using a monopolar or scissors forceps when releasing adhesion, (3) clarify the anatomy around the ureter for cases needing hemostasis, (4) repeatedly confirm the ureter with its peristalsis even after its isolation, (5) for severe adhesion cases, reduce infection risk by drain placement and administering antibiotics, and (6) use a delineator cup.

Allelopathic Substances of Osmanthus spp. for Developing Sustainable Agriculture.

Osmanthus fragrans Lour. has been cultivated for more than 2500 years because of the fragrance and color of the flowers. The flowers and roots have been used in tea, liquors, foods, and traditional Chinese medicine. The species contains more than 180 compounds including terpenoids, phenylpropanoids, polyphenols, flavonoids, and sterols. However, there has been limited information available on the allelopathic properties and allelopathic substances of O. fragrans. We investigated the allelopathy and allelopathic substances of O. fragrans and Osmanthus heterophyllus (G.Don) P.S. Green, as well as Osmanthus × fortunei Carrière, which is the hybrid species between O. fragrans and O. heterophyllus. The leaf extracts of O. fragrans, O. heterophyllus, and O. × fortunei suppressed the growth of cress (Lepidium sativum L.), alfalfa (Medicago sativa L.), Lolium multiflorum Lam., and Vulpia myuros (L.) C.C.Gmel with the extract concentration dependently. The extract of the hybrid species O. × fortune was the most active among the extracts. The main allelopathic substances of O. × fortunei and O. fragrans were isolated and identified as (+)-pinoresinol and 10-acetoxyligustroside, respectively. (+)-Pinoresinol was also found in the fallen leaves of O. × fortunei. Both compounds showed an allelopathic activity on the growth of cress and L. multiflorum. On the other hand, several allelopathic substances including (+)-pinoresinol may be involved in the allelopathy of O. heterophyllus. O. fragrans, O. heterophyllus, and O. × fortunei are evergreen trees. but their senescent leaves fall and cover the soil under the trees. It is possible that those allelopathic substances are liberated through the decomposition process of the leaves into their rhizosphere soil, and that they accumulate in the soil and provide a competitive advantage to the species through the inhibition of the growth of the neighboring competing plants. Therefore, the leaves of these Osmanthus species are allelopathic and potentially useful for weed management options in some agriculture settings to reduce commercial herbicide dependency for the developing sustainable agriculture systems.

Decrease of guanylyl cyclase ß1 subunit and nitric oxide (NO)-induced relaxation in mouse rectum with colitis and its reproduction on long-term NO treatment.

Nitric oxide (NO) influences motility in the colon in patients with ulcerative colitis, but the exact mechanism involved remains unknown. Colitis was induced in mice by the oral administration of 2.5% dextran sodium sulfate (DSS), and the motility in longitudinal preparations from rectum and distal colon and expression of ß1 subunit of soluble guanylyl cyclase (sGCß1) were analyzed. Electrical stimulation (ES) caused a transient relaxation via the NO pathway in both rectum and colon from control mice. Stimulation with sodium nitroprusside (SNP) caused relaxation in the two regions, and the half-time (T (1/2)) of the maximal relaxation induced by 100 µM SNP was 8.1 ± 1.0 s in rectum. DSS treatment (1) abolished the ES-induced relaxation, but not dibutyryl cyclic GMP-induced response, in both regions, (2) decreased the maximal response to SNP accompanied by a loss of immunoreactive sGCß1 protein in rectum, but did not affect the amplitude of the relaxant response or the protein in distal colon, and (3) caused an increase in the T (1/2) value in response to SNP in both regions. Pretreatment of both preparations from control mice with 600 µM SNP for 30 min decreased both ES- and SNP-induced relaxation, SNP-induced cyclic GMP formation, and immunoreactive sGCß1 levels. NO-mediated relaxation was impaired by a dysfunctional sGC with and without a loss of immunoreactivity to sGCß1 in rectum and colon from DSS-treated mice, respectively. Long-term exposure of the tissues with an excess amount of NO changes the sGC-mediated relaxation.

Neurogenic contraction of mouse rectum via the cyclooxygenase pathway: Changes of PGE2-induced contraction with dextran sulfate sodium-induced colitis.

Recent reports suggest that cyclooxygenases (COXs) including COX-2 are constitutively expressed, and prostaglandins (PGs) regulate motility and/or contraction in the colon and rectum. This study examines the role of COXs in the regulation of neuromuscular function in longitudinal preparations of isolated rectum and distal colon (Side A, close to the transverse colon; and Side B, close to the rectum) in normal mice and after the induction of colitis by dextran sulfate sodium (DSS). In control rectum, electrical stimulation (ES)-induced contractions were inhibited by atropine and by COX inhibitors, in an independent manner. PGE(2) at 3microM caused a marked contraction, but the secondary response at 20min after the first application was 60% desensitized. In rectum from DSS-treated mice, spontaneous and ES-induced contractions were significantly less intense than in the control preparations, and the response to PGE(2) was abolished but that to 3microM acetylcholine was not. In control distal colon, the responses to PGE(2) in neither side were desensitized by the repeated application. In DSS-treated distal colon, PGE(2) response was impaired in the two regions, and was desensitized on Side B more than Side A. DSS treatment impaired contractions by 40mM KCl in rectum and on Side B but not Side A. DSS treatment increased COX-2 expression in rectum, but not in distal colon. These findings suggest that the induction of colitis by DSS affects ES- and PGE(2)-regulated motility in the order rectum>distal colon close to the rectum>distal colon in mice.

Nicotine-induced neurogenic relaxation in the mouse colon: changes with dextran sodium sulfate-induced colitis.

Nicotine has been shown to reduce both tone and muscular activity in the human colon by releasing nitric oxide (NO) from nerves. To our knowledge, however, the effect of nicotine on mouse colon has not been elucidated, and the response in tissue from ulcerative colitis (UC) has not been investigated. We examined nicotine-induced responses in colon from control mice and mice with dextran sodium sulfate (DSS)-induced UC. In controls, bath application of nicotine caused a transient relaxation in longitudinal preparations from the transverse and distal colons but not from the rectum. The response was observed in the presence of bethanechol, abolished by treatment with tetrodotoxin and hexamethonium, and mediated partially (>50%) by the NO pathway. In longitudinal preparations of the distal colon from DSS-treated mice, spontaneous contractions decreased markedly, and nicotine caused contraction without relaxation in half of the preparations tested. Nicotine-induced relaxation in the presence of bethanechol was significantly decreased in the DSS-treated distal colon without changing bethanechol-induced contractions. These data suggest that 1) responses to nicotine differ dependent on colon regions, 2) DSS treatment predominantly caused nicotine-sensitive neurogenic changes in distal colon, and 3) DSS treatment may reverse the direction of nicotine-evoked responses in the colon, in mice.

Monomethoxypolyethylene glycol-modified cardiac myosin treatment blocks the active and passive induction of experimental autoimmune myocarditis.

BACKGROUND: Injecting various protein antigens conjugated to monomethoxypolyethylene glycol (mPEG) results in antigen-specific tolerance to subsequent immunization. In the present study the ability of mPEG-modified cardiac myosin (CM) to block the development of experimental autoimmune myocarditis (EAM) induced by CM immunization or by the transfer of lymphocytes from CM-immunized donors was studied. METHODS AND RESULTS: A/J mice were injected with mPEG-CM before active or passive EAM induction. We examined the suppressive mechanism by the transfer of lymphocytes from mPEG-CM-treated mice into naïve mice. To ascertain the cells responsible for suppressing EAM induction, in vivo or in vitro depletion of CD4(+) or CD8(+) T cells was performed. mPEG-CM administered before active or passive EAM induction markedly suppressed the incidence and severity of EAM and reduced CM-specific antibody responses. When lymphocytes from mPEG-CM treated mice were transferred into naïve mice that were then immunized with CM, the suppressive effect was recapitulated. CONCLUSIONS: mPEG-CM treatment blocked the active and passive induction of EAM.