AIMTo cure typically life-threatening esophagogastric anastomosis in rats, lacking anastomosis healing and sphincter function rescue, in particular.METHODSBecause we assume esophagogastric fistulas represent a particular NO-system disability, we attempt to identify the benefits of anti-ulcer stable gastric pentadecapeptide BPC 157, which was in trials for ulcerative colitis and currently for multiple sclerosis, in rats with esophagocutaneous fistulas. Previously, BPC 157 therapies have promoted the healing of intestinal anastomosis and fistulas, and esophagitis and gastric lesions, along with rescued sphincter function. Additionally, BPC 157 particularly interacts with the NO-system. In the 4 d after esophagogastric anastomosis creation, rats received medication (/kg intraperitoneally once daily: BPC 157 (10 μg, 10 ng), L-NAME (5 mg), or L-arginine (100 mg) alone and/or combined or BPC 157 (10 μg, 10 ng) in drinking water). For rats underwent esophagogastric anastomosis, daily assessment included progressive stomach damage (sum of the longest diameters, mm), esophagitis (scored 0-5), weak anastomosis (mL H2O before leak), low pressure in esophagus at anastomosis and in the pyloric sphincter (cm H2O), progressive weight loss (g) and mortality. Immediate effect assessed blood vessels disappearance (scored 0-5) at the stomach surface immediately after anastomosis creation.RESULTSBPC 157 (all regimens) fully counteracted the perilous disease course from the very beginning (i.e., with the BPC 157 bath, blood vessels remained present at the gastric surface after anastomosis creation) and eliminated mortality. Additionally, BPC 157 treatment in combination with L-NAME nullified any effect of L-NAME that otherwise intensified the regular course. Consistently, with worsening (with L-NAME administration) and amelioration (with L-arginine), either L-arginine amelioration prevails (attenuated esophageal and gastric lesions) or they counteract each other (L-NAME + L-arginine); with the addition of BPC 157 (L-NAME + L-arginine + BPC 157), there was a marked beneficial effect. BPC 157 treatment for esophagogastric anastomosis, along with NOS-blocker L-NAME and/or NOS substrate L-arginine, demonstrated an innate NO-system disability (as observed with L-arginine effectiveness). BPC 157 distinctively affected corresponding events: worsening (obtained with L-NAME administration that was counteracted); or amelioration (L-arginine + BPC 157-rats correspond to BPC 157-rats).CONCLUSIONInnate NO-system disability for esophagogastric anastomoses, including L-NAME-worsening, suggests that these effects could be corrected by L-arginine and almost completely eliminated by BPC 157 therapy.

Ovarian vein thrombosis should be taken under consideration in the post-partum period.

No abstract

BACKGROUND:Some benign changes of the ovaries like hyper reaction luteinalis sometimes cannot be differentiated from malignant ones without histological examination. In these cases, surgical intervention sometimes cannot be avoided. Hyperreactio luteinalis is a condition that can occur only in pregnancy. It is characterised by bilateral benign multicystic ovarian enlargement.CASE REPORT:We present a case of misleading intraoperative findings during Cesarean section that ended with ovariectomy.CONCLUSION:During the Caesarean section, some benign masses of the ovaries, like hyper reaction luteinalis, are difficult to differentiate from malignant disease without histological examination, requiring surgical intervention.

SUMMARY Gestational diabetes involves disorder of glucose metabolism first diagnosed in pregnancy. Obese women undoubtedly have more often complications in reproductive age, such as fertility difficulties, spontaneous and recurrent miscarriages, premature births, and various obstetric and surgical complications related to the course of pregnancy, delivery and puerperium. Children of obese pregnant women are more likely to develop obesity in childhood and adulthood. We analyzed the outcome of 51 pregnancies in obese pregnant women and 50 pregnant women with normal body mass index. All women in both groups were diagnosed with gestational diabetes by the IADPSG criteria. We analyzed gestational age at delivery and mode of delivery, gestational weight gain, presence of concomitant diagnosis of gestational or chronic hypertension, difference in birth weight, and prevalence of hypertrophic newborns. There was no significant difference in gestational age at pregnancy termination and in the mode of delivery. There was a significant difference in gestational weight gain, number of pregnant women with hypertension, neonatal birth weight and number of hypertrophic children. Based on the data presented, we conclude that obesity is an unfavorable factor for pregnancy outcome. It also influences birth weight and fetal hypertrophy, as well as gestational weight gain.