Continuous interfacial polycondensation of nylon 6-6

Nylon 6-6 has been prepared by continuous interfacial polycondensation from hexamethylene diamine and adipyl chloride in a stirred system. The effect of monomer concentration and stirring on the intrinsic viscosity of polyamide 6-6 solution in formic acid (90%) was determined. As stirring rate and monomer ratio increased, the intrinsic viscosity and polymer yield went through a maximum. Diffusion coefficient (DAB) for hexamethylene diamine was calculated and from that JD and mass transfer coefficient /DAB were calculated. A relation between Reynolds number and JD factor was established by correlation curve

Study of early perinatal outcome in lower segment caesarean section in severe foetal distress at tertiary care centre

Background: For asphyxia, the fetus reacts with a series of responses. First there is redistribution of blood flow to vital centres to limit the deleterious effects of oxygen limitation in the brain, heart and adrenal glands. A further compensatory response is that overall fetal oxygen consumption declines to values as low as 50% of the control.Methods: This was a prospective study. Early perinatal outcome of newborns delivered through Caesarean section due to clinical foetal distress in labour was compared with a group of newborns similarly delivered via Caesarean section without a diagnosis of clinical foetal distress. Data collected and analysed using appropriate standard statistical methods i.e. Chi-square (X2) test and ‘Z’ - test.Results: Most common indication for NICU admission in study group was MAS (Meconium Aspiration Syndrome 14%) followed by MAS with perinatal asphyxia (5.33%), MAS with Hypoxic ischaemic encephalopathy (HIE) - stage III (3.33%) paerintal asphyxia (2.66%), severe PNA with HIE - III (0.66%) and TTN (0.66%) meconium gastritis (0.66%) respectively.Conclusions: Clinical foetal distress (study group) was found to be significantly associated with low 1 min and 5 min. Apgar score. There was no significant difference in immediate NICU admission whether D-D (i.e. detection fetal detection to delivery interval) time interval 30 minutes. But rate of mortality was high when D-D (i.e. detection fetal detection to delivery interval) was >30 minutes

Immune-inflammation gene signatures in endometriosis patients

To determine if the molecular profiles of endometriotic lesions contain informative measures of inflammation and immune dysfunction that may contribute to better understanding of the interplay between immune dysfunction and inflammation and their contribution to endometriosis pathogenesis

Protein Inhibitor of Activated STAT3 (PIAS3) Is Down-Regulated in Eutopic Endometrium of Women with Endometriosis

Endometriosis is a major cause of chronic pelvic pain and infertility. Activation of STAT3 appears central to the inflammatory phenotype of eutopic endometrium in women with endometriosis. However, the molecular mechanism by which this occurs remains unknown. Our objective is to determine how STAT3 activity is regulated in endometriosis. Protein inhibitor of activated STAT3 (PIAS3) is a negative regulator of STAT3 activity. We examined the levels of PIAS3 in endometrium from women with and without endometriosis using Western blot analysis and immunohistochemistry. Levels of PIAS3 are significantly lower, in contrast with phosphorylation of STAT3, in women with endometriosis compared to women without endometriosis. Furthermore, induction of endometriosis in the baboon showed a significant reduction of PIAS3 expression during the progression of the disease. Interferon-γ (INFγ) reduces PIAS3 protein levels and increases phospho-STAT3 levels through CXCL10 in endometrial cells, Ishikawa, and 12Z cells. These results suggest that attenuation of PIAS3 causes aberrant activation of STAT3 in endometriosis, leading to inflammatory changes that may impair fertility or cause pain

On the stability of the conduction regime of natural convection in a vertical slot

The stability of the conduction regime of natural convection in a vertical slot has been studied analytically. For Pr Pr > 12.7 the instability sets in as a travelling wave. As the Prandtl number is increased the onset of instability approaches the correct limiting solution which is constant as a function of GrPr1/2.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/33827/1/0000084.pd

Surgical removal of endometriotic lesions alters local and systemic proinflammatory cytokines in endometriosis patients

To determine the impact of endometriotic lesion removal on local and systemic inflammation

Fine Selmer Groups and Isogeny Invariance

We investigate fine Selmer groups for elliptic curves and for Galois representations over a number field. More specifically, we discuss Conjecture A, which states that the fine Selmer group of an elliptic curve over the cyclotomic extension is a finitely generated $\mathbb{Z}_p$-module. The relationship between this conjecture and Iwasawa's classical $\mu=0$ conjecture is clarified. We also present some partial results towards the question whether Conjecture A is invariant under isogenies.Comment: 20 page

Interleukin-33 modulates inflammation in endometriosis

Abstract Endometriosis is a debilitating condition that is categorized by the abnormal growth of endometrial tissue outside the uterus. Although the pathogenesis of this disease remains unknown, it is well established that endometriosis patients exhibit immune dysfunction. Interleukin (IL)-33 is a danger signal that is a critical regulator of chronic inflammation. Although plasma and peritoneal fluid levels of IL-33 have been associated with deep infiltrating endometriosis, its contribution to the disease pathophysiology is unknown. We investigated the role of IL-33 in the pathology of endometriosis using patient samples, cell lines and a syngeneic mouse model. We found that endometriotic lesions produce significantly higher levels of IL-33 compared to the endometrium of healthy, fertile controls. In vitro stimulation of endometrial epithelial, endothelial and endometriotic epithelial cells with IL-33 led to the production of pro-inflammatory and angiogenic cytokines. In a syngeneic mouse model of endometriosis, IL-33 injections caused systemic inflammation, which manifested as an increase in plasma pro-inflammatory cytokines compared to control mice. Furthermore, endometriotic lesions from IL-33 treated mice were highly vascularized and exhibited increased proliferation. Collectively, we provide convincing evidence that IL-33 perpetuates inflammation, angiogenesis and lesion proliferation, which are critical events in the lesion survival and progression of endometriosis

KRAS Activation and over-expression of SIRT1/BCL6 Contributes to the Pathogenesis of Endometriosis and Progesterone Resistance

Endometriosis is an inflammatory condition that is associated with progesterone resistance and cell proliferation, resulting in pain, infertility and pregnancy loss. We previously demonstrated phosphorylation of STAT3 in eutopic endometrium of infertile women with this disorder leading to over-expression of the oncogene BCL6 and stabilization of hypoxia-induced factor 1 alpha (HIF-1α). Here we report coordinated activation of KRAS and over-expression of Sirtuin 1 (SIRT1), a histone deacetylase and gene silencer, in the eutopic endometrium from women with endometriosis throughout the menstrual cycle. The mice with conditional activation of KRAS in the PGR positive cells reveal an increase of SIRT1 expression in the endometrium compared to control mice. The expression of progesterone receptor target genes including the Indian Hedgehog pathway genes are significantly down-regulated in the mutant mice. SIRT1 co-localizes with BCL6 in the nuclei of affected individuals and both proteins bind to and suppress the promoter of GLI1, a critical mediator of progesterone action in the Indian Hedgehog pathway, by ChIP analysis. In eutopic endometrium, GLI1 expression is reduced in women with endometriosis. Together, these data suggest that KRAS, SIRT1 and BCL6 are coordinately over-expressed in eutopic endometrium of women with endometriosis and likely participate in the pathogenesis of endometriosis