Correlation between increased maternal body mass index and pregnancy complications.

OBJECTIVE: Obesity in pregnancy carries significant maternal and fetal risk. The aim of this study was to investigate the effect of maternal body mass index on pregnancy outcomes. PATIENTS AND METHODS: The study retrospectively reviewed the clinical outcome of 485 pregnant women who delivered at the Department of Obstetrics and Gynecology, Clinical Centre of Vojvodina, Novi Sad, during the period of three years (2018-2020) and compared them against the body mass index (BMI). Correlation coefficient was calculated for BMI and seven pregnancy complications (hypertensive syndrome, preeclampsia, gestational diabetes mellitus, intrauterine growth restriction, premature rupture of membranes, mode of delivery and postpartum hemorrhage). The collected data were presented in the form of median values and relative numbers (the measure of variability). The implementation of the simulation model and its verification were carried out using a specialized programming language, Python. Statistical models were created where the Chi-square and p-value were as determined for every observed outcome. RESULTS: The average age of the subjects was 35.79 years and average BMI 29.28 kg/m2. A statistically significant correlation was found between the BMI and arterial hypertension, gestational diabetes mellitus, preeclampsia and cesarean section. The correlations between the body mass index and postpartum hemorrhage, intrauterine growth restriction and premature rupture of membranes were not statistically significant. CONCLUSIONS: As high BMI correlates with a number of negative outcomes in pregnancy, weight control before and during pregnancy and proper antenatal and intranatal care are necessary to achieve a favorable pregnancy outcome.

Yeast exocytic v-SNAREs confer endocytosis.

In yeast, homologues of the synaptobrevin/VAMP family of v-SNAREs (Snc1 and Snc2) confer the docking and fusion of secretory vesicles at the cell surface. As no v-SNARE has been shown to confer endocytosis, we examined whether yeast lacking the SNC genes, or possessing a temperature-sensitive allele of SNC1 (SNC1(ala43)), are deficient in the endocytic uptake of components from the cell surface. We found that both SNC and temperature-shifted SNC1(ala43) yeast are deficient in their ability to deliver the soluble dye FM4-64 to the vacuole. Under conditions in which vesicles accumulate, FM4-64 stained primarily the cytoplasm as well as fragmented vacuoles. In addition, alpha-factor-stimulated endocytosis of the alpha-factor receptor, Ste2, was fully blocked, as evidenced using a Ste2-green fluorescent protein fusion protein as well as metabolic labeling studies. This suggests a direct role for Snc v-SNAREs in the retrieval of membrane proteins from the cell surface. Moreover, this idea is supported by genetic and physical data that demonstrate functional interactions with t-SNAREs that confer endosomal transport (e.g., Tlg1,2). Notably, Snc1(ala43) was found to be nonfunctional in cells lacking Tlg1 or Tlg2. Thus, we propose that synaptobrevin/VAMP family members are engaged in anterograde and retrograde protein sorting steps between the Golgi and the plasma membrane.

Neomycin--a frequent contact allergen.

The incidence of allergic contact dermatitis from neomycin evaluated in relation to 1381 verified cases of allergic contact dermatitis showed a progressive increase (5.00, 7.69, 10.18%) over a three-year period (1990-1992). Sensitivity to neomycin was investigated with special reference to possible cross-reactions between neomycin and the allergens that are commonly used in the manufacture of cosmetic products. Contact sensitivity to neomycin was found to be present with the other diagnoses, such as atopic dermatitis, seborrhoeic dermatitis, hypostasic dermatitis and psoriasis vulgaris.

Norepinephrine stimulates the direct breakdown of phosphatidyl inositol in rat tail artery.

When segments of rat tail artery were labeled with [3H]inositol and then stimulated with norepinephrine (NE), the inositol phosphates produced were primarily IP and IP2, together with a small but significant amount of Ins(1,4,5)P3 and a very small amount of Ins(1,3,4,5)P4. It has been unclear in many studies whether or not the relatively large levels of IP and IP2 produced in [3H]inositol-labeled tissue represent indirect products of phosphatidyl inositol(4,5)bis phosphate breakdown (through Ins(1,4,5)P3) or direct products of phosphatidyl inositol 4 monophosphate and phosphatidyl inositol breakdown. In order to answer this question tail artery segments were prelabeled with [3H]inositol and then permeabilized with beta escin and stimulated with norepinephrine and GTP gamma S, so that increases in IP, IP2, and Ins(1,4,5)P3 were still observed. If these permeable segments were stimulated with agonist in the presence of compounds known to inhibit Ins(1,4,5)P3 5-phosphatase, such as glucose 6P, (2,3)diphosphoglycerate, or Ins(1,4,5)P3, the levels of labeled Ins(1,4,5)P3 and labeled IP2 were increased, while the level of stimulated labeled IP was unchanged. This indicated that some of the IP2 and IP formed in these cells was produced from PIP2 but that some of these compounds might be formed from PIP or PI. When the isomers of inositol monophosphate, Ins 1P and Ins 4P, were separated by HPLC, it was shown that after prelabeled tail artery was stimulated by norepinephrine for periods of 1-2 min, the predominant isomer formed was Ins 4P, indicating either PIP2 or PIP as the source. However, after 5-20 min stimulation, both Ins 1P and Ins 4P were formed in equal amounts, suggesting that during sustained stimulation of smooth muscle PI itself was broken down directly. Therefore it appears that within 1-2 min of norepinephrine addition to vascular smooth muscle the bulk of the IP and IP2 produced are derived from PIP2 via IP3, while after 20 min of norepinephrine treatment much of the IP comes directly from PI. This suggests that the regulation of PLC in this tissue is more complicated than has been previously believed.

Norepinephrine-induced phosphatidylcholine hydrolysis by phospholipases D and C in rat tail artery.

Rat tail arterial segments were incubated with [3H]choline to selectively label endogenous phosphatidylcholine. Norepinephrine (NE; 10(-5) M) addition for periods of 10 s to 30 min significantly increased the concentration of extracellular phosphatidylcholine metabolites, [3H]choline, and [3H]phosphocholine. The release of [3H]choline and [3H]phosphocholine from the segments was NE dose dependent (10(-6)-10(-3) M). NE also increased the formation of [3H]phosphatidylethanol in [3H]myristate-labeled tail artery in the presence of ethanol, characteristic of phospholipase D activity. NE-induced phosphatidylcholine hydrolysis was blocked by pretreatment with prazosin (10(-5) M) and was unchanged by pretreatment with propranolol (10(-5) M). 4 beta-phorbol 12,13-dibutyrate (PDBu, 10(-6) M) stimulated the release of [3H]choline, which was inhibited by pretreatment with staurosporine (10(-5) M). The stimulatory effect of NE on phosphatidylcholine metabolism was not altered by either pretreatment with staurosporine (10(-5) M) or calcium-free buffer. In summary, we have demonstrated NE-stimulated phosphatidylcholine hydrolysis by phospholipase D and C in intact vascular smooth muscle. This effect of NE was dose dependent and was mediated through the alpha 1-adrenergic receptor. Norepinephrine and PDBu stimulated phosphatidylcholine hydrolysis through different mechanism(s), and the stimulatory effect of NE did not seem to require protein kinase C and calcium influx.