We investigated the vascular effects of glucagon-like peptide-1 (GLP-1) and Exendin-4 in type 2 diabetic rat aortae. Studies were performed in a normal control group (NC) (0.2 ml i.p. saline, n = 10), streptozotocin (STZ)/nicotinamide diabetic control group (DC) (a single dose of 80 mg/kg STZ i.p. injection 15 min after administration of 230 mg/kg nicotinamide i.p.), GLP-1 (GLPC) control group (1 µg/kg twice daily i.p. for 1 month, n = 10), Exendin-4 control group (EXC) (0.1 µg/kg twice daily i.p. for 1 month, n = 10), GLP-1-treated diabetic group (GLPT) (1 µg/kg twice daily i.p. for 1 month, n = 10), and Exendin-4-treated diabetic group (EXT) (0.1 µg/kg twice daily i.p. for 1 month, n = 10). One month of GLP-1 and Exendin-4 treatment significantly decreased the blood glucose levels of diabetic rats (113 ± 2 mg/dl, p < 0.001, and 117 ± 1 mg/dl, p < 0.001, respectively versus 181 ± 9 mg/dl in the DC group). Sensitivity (pD2) and maximum response (% Max. Relax) of acetylcholine-stimulated relaxations in the DC group (pD2: 6.73 ± 0.12 and 55 ± 6, respectively) were decreased compared with the non-diabetic NC group (pD2: 7.41 ± 0.25, p < 0.05, and 87 ± 4, p < 0.01). Treating diabetic rats with GLP-1, pD2 values and with Exendin-4, Max. Relax %values of aortic strips to acetylcholine returned to near non-diabetic NC values (pD2: 7.47 ± 0.15, p < 0.05, and 87 ± 3, p < 0.01, respectively). Maximal contractile responses (Emax) to noradrenaline in aortic strips from the diabetic DC group (341 ± 27 mg tension/mg wet weight) were significantly decreased compared with the non-diabetic NC (540 ± 66 mg tension/mg wet weight, p < 0.001) and the GLPT group (490 ± 25 mg tension/mg wet weight, p < 0.05). There were no significant differences in pD2 values of aortic strips to noradrenaline from all groups. Emax to KCl in aortic strips from the DC group (247 ± 10 mg tension/mg wet weight, p < 0.01) was significantly decreased compared with non-diabetic NC group (327 ± 26 mg tension/mg wet weight). Treating diabetic rats with GLP-1 (GLPT), Emax values of aortic strips to KCl returned to near non-diabetic NC values (271 ± 12 mg tension/mg wet weight). GLP-1 and (partially) Exendin-4 treatment could improve the increased blood glucose level and normalize the altered vascular tone in type 2 diabetic rats.

There is a paucity of data on whether pre-operative walking and functional capacity has a direct association with post-operative gastrointestinal function in patients who have undergone surgery to treat gynecologic cancers. To explore the relationship between pre-operative walking and post-operative recovery of bowel function. This randomized trial was performed from January 1, 2018 to August 31, 2018. All patients had a diagnosis of endometrial or ovarian cancer and were scheduled for comprehensive staging. Group A served as the control group who did not walk regularly on the last night before surgery. Patients in group B walked for 30 min at an average speed of 3 km/h from 20.00 to 20.30 and 21.30. to 22.00 on the last night before surgery under the supervision of a nurse or doctor. The study was registered with clinicaltrials.gov (no: NCT03553121). A total of 85 patients were enrolled: 43 patients were assigned to the walking group and 42 to the control group. There were no significant differences in demographics between the groups. Median age was 57.3±8.5 in the control and 59.9±9.1 in the walking group. In addition, 28 patients had endometrial cancer and 14 had ovarian cancer in the control group. 33 patients and 10 patients in the walking group had endometrial and ovarian cancer, respectively. The mean time to first flatus was shorter in the walking group than in the control group (32.5±10.4 vs 40.6±16.9 hours, respectively; p=0.010). In addition, the time to first defecation was significantly shorter in the walking group (62.8±26.7 vs 91.4±51.8 hours; p=0.002). Patients who walked before surgery were less likely to have post-operative paralytic ileus (25.0% vs 60.7%; p=0.003). Walking before the operative period and laparoscopic surgery independently protected against the development of post-operative paralytic ileus. Walking before surgery expedited time to bowel motility and ability to tolerate food. In addition, this method significantly decreased the risk of post-operative paralytic ileus.We consider that walking before surgery may be integrated into the pre-operative management of patients under going surgery for gynecologic cancers. clinicaltrial.org record number: NCT03553121.

3D seismic data and wireline logs from 17 wells in the onshore East Nile Delta were utilized to study the stratigraphic architecture and evolution of Oligocene deposits. The Oligocene is readily recognized on seismic cross-sections by a series of northward prograding clinoforms. The Oligocene sequences show lateral facies changes from fluvial to deepwater via a shelf-edge delta. Such deltaic features include distributary channels, interdistributary bay fill, and a delta plain and front, gradually changing downslope into prodelta and slope deposits. The slope deposits include three main depositional elements: a deeply incised channel, a complex of laterally switched leveed channels and lobes, and crevasses and frontal splays. These depositional elements are formed in the main western slope basin and local eastern intraslope ponded sub-basin. The reactivated E–W- and NW-trending faults as well as NE–SW inverted structures are the main controls on slope physiography that formed the main corridors for Oligocene sediment distribution. Two main globally correlated Oligocene sequences are encountered being separated by the major drop in global eustatic sea level at 28.1Ma. The lower Oligocene sequence has two main stages: (1) the formation and filling of a basal canyon; and (2) the formation and progradation of shelf deltas to form shelf-edge deltas, and then progradation with an ascending shelf-edge trajectory (clinoforms 1). The upper Oligocene sequence is characterized by accretionary shelf-edge deltas with descending and then flat trajectories (clinoforms 2–4). The frontal splay and lobe complex exhibits potentially favourable reservoir continuity and areal coverage followed by the slope channels.

Background: Oncostatin M, a novel adipokine, plays a role in oogenesis, lipogenesis, and inflammation and may contribute to polycystic ovary syndrome pathogenesis and related metabolic problems. Adipokines are believed to contribute to developing polycystic ovary syndrome and its accompanying metabolic parameters, such as dyslipidemia, insulin resistance, and cardiovascular diseases. Methods: In this case–control study, the patients were grouped in a 1:1 ratio into either the polycystic ovary syndrome (n = 32) or the control group (n = 32). Serum levels of fasting glucose, insulin, C-reactive protein, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglyceride, white blood cell count, thyroid-stimulating hormone, luteinizing hormone, follicle-stimulating hormone, total testosterone, prolactin, estradiol, homeostasis model assessment of insulin resistance, and oncostatin M were analyzed. Results: Oncostatin M levels were significantly lower, but C-reactive protein levels were substantially higher in the polycystic ovary syndrome group than in the control group (p = 0.002, p = 0.001, respectively). Oncostatin M was inversely correlated with total cholesterol, non-high-density lipoprotein cholesterol, fasting glucose, and the luteinizing hormone/follicle-stimulating hormone ratio (ρ = −0.329, p =0.017; ρ = −0.386, p = 0.005; ρ = −0.440, p = 0.001; ρ = −0.316, p = 0.023, respectively). Conversely, there was no correlation between oncostatin M and total testosterone level (ρ = 0.220; p = 0.118). In the context of inflammation and metabolic parameters, oncostatin M was inversely correlated with C-reactive protein, homeostatic model assessment for insulin resistance score, and low-density lipoprotein cholesterol (ρ = −0.353, p = 0.019; ρ = −0.275, p = 0.048; ρ = −0.470, p < 0.001, respectively). Conclusions: Plasma oncostatin M levels were considerably lower in patients with polycystic ovary syndrome than in the control group, and this was inversely correlated with the hormonal and metabolic parameters of polycystic ovary syndrome. Thus, oncostatin M may be a novel therapeutic target for polycystic ovary syndrome and its metabolic parameters.

Objective: The current study aimed to delineate the relationship between furin and chronic inflammation while cervical intraepithelial neoplasia progresses to cancer. Study Design: This cross-sectional study included 81 women who required colposcopic examinations. The study groups were formed based on pathological results: Group I included women with cervical intraepithelial neoplasia (CIN) I (n = 30); Group II included women with CIN II-III (n = 28); and Group III included women with cervical cancer (CC) (n = 23). Furin, ki-67, and p16 levels were evaluated based on immunostaining intensity. The inflammatory indices were calculated in parallel with the literature from routine blood samples retrieved within one week before the procedure. Results: Furin expression gradually increased from CIN I to CIN II-III and from CIN II-III to CC, respectively (p < 0.001, p = 0.005). NLR, MLR, PLR, and SII were significantly higher in the CC group (p < 0.001). ROC curve analysis unveiled that NLR, MLR, PLR, and SII predicted the presence of CC with a cutoff value of 2.39 for NLR (sensitivity: 91.3%, specificity: 63.8%, AUROC: 0.79, p < 0.001); a cutoff value of 0.27 for MLR (sensitivity: 78.3%, specificity: 72.4%, AUROC: 0.77, p = 0.009); a cutoff value of 123 for PLR (sensitivity: 100%, specificity: 41.4%, AUROC: 0.70, p = 0.04); and a cutoff value of 747 for SII (sensitivity: 69.6%, specificity: 90.7%, AUROC: 0.71, p = 0.014). Conclusion: Furin expression increased gradually in parallel with the severity of cervical intraepithelial neoplasia. The inflammatory indices were higher in the presence of CC and denoted a good discrimination ability for predicting cervical cancer.