Uterine rupture: A review of 15 Cases at Bandier maternity hospital in Somalia

Background: Uterine rupture is a deadly obstetrical emergency endangering the life of both mother and fetus.Objective: To determine the frequency of ruptured uterus at Bandier Hospital and to elicit possible causes and type of management. Methods: It was cross sectional and hospital based descriptive study implemented during a time period of six months (July – December 2013) in Bandier maternity hospital and a total of 15 women presented with rupture uterus during the period of the study were included.Results: There were 15 cases of ruptured uterus out of a total of 2142 deliveries. Incidence of uterine rupture was found to be 0.7%. The mean age of women was 30.03 ± 4.55 years. Concerning risk factors for rupture uterus, 10 (66.7%) had previous uterine surgery, obstructed labor was found in 33.3%, and oxytocin was used in 46.7% of respondents. Repair was done for 8 (53.3%), 3 (20.6%) of respondents underwent total abdominal hysterectomy and 4 (26.7%) were ended by subtotal hysterectomy. Conclusions: Previous uterine surgery, obstructed labour and improper use of oxytocin increase the risk of uterine rupture in this study. Half of the patients underwent hysterectomy

Synthesis, Structural Characterization and Theoretical Investigations of New Azo-Azomethine Compounds Bearing Acryloyl Moiety

I n this study six new azo-azomethine dyes containing acryloyl group, 4-[[[4-[4′-methyl phenyl azo phenyl] imino] methyl] phenyl-2-propenoat, 4-[[[4-[4′- hydroxy phenylazo phenyl] imino] methyl] phenyl-2-propenoat, 4-[[[4- phenyl azo phenyl] imino] methyl]- phenyl-2-propenoat, 4-[[[4-[4′-chloro phenyl azo phenyl] imino] methyl] phenyl-2-propenoat, 4-[[[4-[4′- nitro phenyl azo phenyl] imino] methyl] phenyl-2propenoat were synthesized. The acryloyl derivatives of the azo-azomethine dyes were prepared with metallic sodium and acryloyl chloride in 1:1 Molar ratio and characterized using elemental analysis, IR, UV-Vis, 1H-NMR and 13C-NMR spectroscopy. The molecular geometry was also optimized using density functional theory DFT/B3LYP method with the 6-311G 2d,2p and cc-pvtz basis sets in ground state. From the optimized geometry of the compounds, vibrational frequencies, UV-Vis, molecular electrostatic potential distribution and frontier molecular orbitals were performed using same method and basis stets, and the results were compared with the experimental dat

Antiperoxidative and anti-apoptotic effects of lycopene and ellagic acid on cyclophosphamide-induced testicular lipid peroxidation and apoptosis

The present study was conducted to investigate the possible protective effects of lycopene (LC) and ellagic acid (EA) on cyclophosphamide (CP)-induced testicular and spermatozoal toxicity associated with the oxidative stress and apoptosis in male rats. Forty-eight healthy adult male Sprague-Dawley rats were divided into six groups of eight rats each. The control group was treated with placebo; the LC, EA and CP groups were given LC (10 mg kg−1), EA (2 mg kg−1) and CP (15 mg kg−1), respectively, alone; the CP+LC group was treated with a combination of CP (15 mg kg−1) and LC (10 mg kg−1); and the CP+EA group was treated with a combination of CP (15 mg kg−1) and EA (2 mg kg−1). All treatments were maintained for 8 weeks. At the end of the treatment period, bodyweight and the weight of the reproductive organs, sperm concentration and motility, testicular tissue lipid peroxidation, anti-oxidant enzyme activity and apoptosis (i.e. Bax and Bcl-2 proteins) were determined. Administration of CP resulted in significant decreases in epididymal sperm concentration and motility and significant increases in malondialdehyde levels. Although CP significantly increased the number of Bax-positive (apoptotic) cells, it had no effect on the number of Bcl-2-positive (anti-apoptotic) cells compared with the control group. However, combined treatment of rats with LC or EA in addition to CP prevented the development of CP-induced lipid peroxidation and sperm and testicular damage. In conclusion, CP-induced lipid peroxidation leads to structural and functional damage, as well as apoptosis, in spermatogenic cells of rats. Both LC and EA protect against the development of these detrimental effects

Attenuating effect of lycopene and ellagic acid on 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced spermiotoxicity and testicular apoptosis

This study was conducted to investigate the prophylactic effects of lycopene (LC) and ellagic acid (EA) on 2,3,7,8- tetrachlorodibenzo-p-dioxin (TCDD)-induced testicular and spermatozoal toxicity. These toxicological changes are associated with the oxidative stress and apoptosis in male rats. Forty-eight male rats were allocated to one of six groups of 8 rats each: control, LC, EA, TCDD, TCDD+LC, and TCDD+EA. The control group was treated with 0.5 mL/ rat slightly alkaline solution+0.5 mL/rat corn oil every other day. The LC group was treated with 0.5 mL/rat slightly alkaline solution+0.5 mL/rat corn oil containing 10 mg/kg of LC every other day. The EA group received 0.5 mL/rat corn oil+0.5 mL/rat slightly alkaline solution containing 2 mg/kg of EA every other day. The TCDD group received 0.5 mL/rat corn oil containing 100 ng/kg/day of TCDD+0.5 mL/rat slightly alkaline solution. The TCDD+LC group was treated with 0.5 mL/rat TCDD+0.5 mL/rat LC. The TCDD+EA group was treated with 0.5 mL/rat TCDD+0.5 mL/rat EA. All treatments were made by gavage, and the experimental period was maintained during 8 weeks. Sperm motility, concentration, and abnormal sperm rate in epididymal tissue, testicular tissue lipid peroxidation (LPO), antioxidant enzyme activity, histopathological changes, and apoptosis (i.e., Bax and Bcl-2 proteins) were determined. TCDD exposure resulted in significant decreases in sperm motility, concentration, testicular superoxide dismutase activity, germinal cell-layer thickness, Johnsen’s testicular score, and significant increases in abnormal sperm rate, testicular malondialdehyde, glutathione levels, Bax-positive staining, and Bax-positive apoptotic cell score, along with some testicular histopathological lesions. TCDD treatment did not affect significantly catalase activity. However, combined treatment with LC or EA, in addition to TCDD, prevented the development of TCDD-induced damages in sperm quality, testicular histology, and LPO. Improvements in testicular apoptosis after the administration of LC and EA to TCDD-treated rats were minimal, but not statistically significant. TCDD-induced lipid peroxidation leads to functional and structural damages, as well as apoptosis, in spermatogenic cells of rats. Both LC and EA protected against the development of these effect

Protective effects of curcumin on antioxidant status, body weight gain, and reproductive parameters in male rats exposed to subchronic 2,3,7,8-tetrachlorodibenzo-p-dioxin

The aim of this study was to investigate the effects of curcumin (CUR) on antioxidant status, body weight (BW) gains, and some reproductive parameters in male rats exposed to subchronic doses of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Thirtytwo rats were divided into four groups. The first group was kept as control. The second group (TCDD group) was given TCDD at a dose of 50 ng kg 1 BW per day; the third group (CUR group) was treated with CUR at a dose of 80 mg kg 1 BW per day. The fourth group (TCDD þ CUR group) was given TCDD and CUR at the same doses simultaneously. Malondialdehyde (MDA) levels were significantly increased in the TCDD group. In addition, TCDD exposure decreased liver superoxide dismutase (SOD) activity, catalase (CAT) activities of kidney and brain, glutathione peroxidase (GSH-Px) activities of liver, kidney, and brain, and glutathione levels of liver, kidney, and heart. However, CUR treatment with TCDD exposure decreased MDA levels in all tissues and increased SOD activities of liver, kidney, and brain, CAT activity of heart, and GSH-Px activities of heart and brain. TCDD caused a decrease in BW gain, and CUR partially eliminated this effect of TCDD. In addition, while reproductive organ weights, sperm concentration, and sperm motility tended to decrease with TCDD exposure, these effects tended to be close to normal levels by CUR treatment. In conclusion, CUR was seen to be effective in the treatment and prevention of toxicity induced by subchronic TCDD exposure

Amplification of the 20q Chromosomal Arm Occurs Early in Tumorigenic Transformation and May Initiate Cancer

Duplication of chromosomal arm 20q occurs in prostate, cervical, colon, gastric, bladder, melanoma, pancreas and breast cancer, suggesting that 20q amplification may play a causal role in tumorigenesis. According to an alternative view, chromosomal imbalance is mainly a common side effect of cancer progression. To test whether a specific genomic aberration might serve as a cancer initiating event, we established an in vitro system that models the evolutionary process of early stages of prostate tumor formation; normal prostate cells were immortalized by the over-expression of human telomerase catalytic subunit hTERT, and cultured for 650 days till several transformation hallmarks were observed. Gene expression patterns were measured and chromosomal aberrations were monitored by spectral karyotype analysis at different times. Several chromosomal aberrations, in particular duplication of chromosomal arm 20q, occurred early in the process and were fixed in the cell populations, while other aberrations became extinct shortly after their appearance. A wide range of bioinformatic tools, applied to our data and to data from several cancer databases, revealed that spontaneous 20q amplification can promote cancer initiation. Our computational model suggests that 20q amplification induced deregulation of several specific cancer-related pathways including the MAPK pathway, the p53 pathway and Polycomb group factors. In addition, activation of Myc, AML, B-Catenin and the ETS family transcription factors was identified as an important step in cancer development driven by 20q amplification. Finally we identified 13 "cancer initiating genes", located on 20q13, which were significantly over-expressed in many tumors, with expression levels correlated with tumor grade and outcome suggesting that these genes induce the malignant process upon 20q amplification

Pore timing:the evolutionary origins of the nucleus and nuclear pore complex

The name “eukaryote” is derived from Greek, meaning “true kernel”, and describes the domain of organisms whose cells have a nucleus. The nucleus is thus the defining feature of eukaryotes and distinguishes them from prokaryotes (Archaea and Bacteria), whose cells lack nuclei. Despite this, we discuss the intriguing possibility that organisms on the path from the first eukaryotic common ancestor to the last common ancestor of all eukaryotes did not possess a nucleus at all—at least not in a form we would recognize today—and that the nucleus in fact arrived relatively late in the evolution of eukaryotes. The clues to this alternative evolutionary path lie, most of all, in recent discoveries concerning the structure of the nuclear pore complex. We discuss the evidence for such a possibility and how this impacts our views of eukaryote origins and how eukaryotes have diversified subsequent to their last common ancestor

Integrating Human-Centred Design Approach into Sustainable-Oriented 3D Printing Systems

Modern 3D printing systems have become pervasive and widely used both in professional and in informal contexts, including sustainable-oriented ones. However, the risk to create very effective but non-sustainable solutions is very high since 3D printing systems could potentially increase the environmental emergencies and the unsustainable growth. In the transition process toward sustainable ways of production and consumption, the so-called human factor still plays an important role in the achievement of sustainable-oriented actions; it drives the adoption of proper lifestyles that directly and indirectly influence the ways through which such technologies are used. Therefore, future Sustainable 3D Printing Systems should integrate the humans in the systems’ development. This study presents two important results: (a) it presents a set of interdisciplinary ‘Sustainable 3D Printing Systems’, which compose a promising sustainable-oriented scenario useful to support the transition processes toward sustainable designs and productions, and (b) it proposes a new strategy for the integration of human-centred aspects into Sustainable 3D Printing Systems, by combining insights from human-centred design approach

Matched pairs of human prostate stromal cells display differential tropic effects on LNCaP prostate cancer cells

Prostate stromal cells may play binary roles in the process of prostate cancer development. As the first to be encountered by infiltrating prostate cancer cells, prostate stromal cells form the first defense line against prostate cancer progression and metastasis. However, interaction between prostate cancer and stromal cells may facilitate the formation of a tumor microenvironment favoring cancer cell growth and survival. To establish an experimental system for studying the interaction between cancer and stromal cells, we isolated three matched pairs of normal and cancer-associated human prostate stromal clones. In this report, we describe the morphologic and behavioral characteristics of these cells and their effect on LNCaP prostate cancer cells in co-culture. Unlike LNCaP prostate cancer cells, the isolated prostate stromal clones are large fibroblast-like cells with a slow proliferation rate. Growth and survival of these clones are not affected by androgens. The stromal cells display high resistance to serum starvation, while cancer-associated stromal clones have differentiated survival ability. In co-culture experiments, the stromal cells protected some LNCaP prostate cancer cells from death by serum starvation, and cancer-associated stromal clones showed more protection. This work thus established a panel of valuable human prostate stromal cell lines, which could be used in co-culture to study the interaction between prostate cancer and prostate stromal cells