84 research outputs found

    Dealing a Neonate with CHARGE Syndrome: Anaesthesia perspective of perioperative care

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    CHARGE syndrome is a condition that can disturb numerous areas of human body. As an abbreviation CHARGE stands for: coloboma, heart defects, atresia choanae, and retardation of growth, genital, and ear abnormalities. The configuration of malformations differs among individuals with this disorder, and the various health issues can be life-threatening during infancy and childhood. Affected individuals typically have several main features or a combination of major and minor appearances. Here we are presenting a case report of a neonate with CHARGE syndrome who underwent successful repair of choanal atresia under general anaesthesia with invasive monitoring

    Methyl 4-{[(4-methyl­phen­yl)sulfon­yl]amino}­benzoate

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    In the mol­ecule of the title compound, C15H15NO4S, the dihedral angle between the two rings is 88.05 (7)°. The methyl ester group is nearly coplanar with the adjacent ring [dihedral angle = 2.81 (10)°], whereas it is oriented at 86.90 (9)° with respect to the plane of the ring attached to the –SO2– group. Weak intra­molecular C—H⋯O hydrogen bonding completes S(5) and S(6) ring motifs. The mol­ecules form one-dimensional polymeric C(8) chains along the [010] direction due to N—H⋯O hydrogen bonding and these chains are linked by C—H⋯O hydrogen bonds, forming a three-dimensional network

    4-Methyl-N-{4-[(5-methyl-1,2-oxazol-3-yl)sulfamo­yl]phen­yl}benzene­sulfonamide

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    In the title compound, C17H17N3O5S2, the dihedral angle between the two benzene rings is 81.27 (8)° and the heterocyclic ring is oriented at 9.1 (2) and 76.01 (9)° with respect to these rings. Mol­ecules are connected via N—H⋯N and N—H⋯O hydrogen bonds, generating an R 2 2(8) motif, into chains running along the [001] direction. There is also an intra­molecular C—H⋯O hydrogen bond completing an S(6) ring motif. The polymeric chains are inter­linked through inter­molecular C—H⋯O hydrogen bonds

    4-[2-(Anthracen-9-yl­methyl­idene)hydrazinyl­idene]-3-chloro-1-methyl-3,4-dihydro-1H-2λ6,1-benzothia­zine-2,2-dione

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    In the title compound, C24H18ClN3O2S, the dihedral angle between the benzene ring and the anthracene ring system is 41.10 (8)°. The thia­zine ring has a half-chair conformation and the Cl atom is in an axial orientation. In the crystal, mol­ecules are linked by C—H⋯O inter­actions, generating C(8) chains along [100]. A C—H⋯N short contact occurs in the mol­ecule, generating an S(6) ring

    6-Bromo-1-methyl-1H-2,1-benzothia­zin-4(3H)-one 2,2-dioxide

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    In the crystal structure of the title compound, C9H8BrNO3S, the thia­zine ring is in the twisted form. In the crystal, pairs of inter­molecular C—H⋯O hydrogen bonds form inversion dimers with an R 2 2(8) ring motif. Weak inter­molecular C—H⋯Br and C—H⋯π inter­actions are also present

    A triclinic polymorph of N-[4-(4-methyl­benzene­sulfonamido)­phenyl­sulfon­yl]acetamide

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    In the asymmetric unit of the title compound, C15H16N2O5S2, there are two symmetry-independent mol­ecules which adopt similar conformations, with dihedral angles between the aromatic rings of 59.30 (8) and 61.81 (8)°, and dihedral angles between acetamide group and the benzene ring of 77.08 (10) and 78.40 (10)°. Each type of mol­ecule forms similar one-dimensional polymeric structures extending along the b axis via N—H⋯O hydrogen bonds. These hydrogen bonds generate two types of centrosymmetric motifs, R 2 2(8) and R 2 2(20). Moreover C—H⋯O inter­actions assemble the mol­ecules into a three-dimensional framework. The crystal structure was determined from a non-merohedral twin [ratio of the twin components = 0.322 (4):0.678 (4)]

    Keratins Are Altered in Intestinal Disease-Related Stress Responses

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    Keratin (K) intermediate filaments can be divided into type I/type II proteins, which form obligate heteropolymers. Epithelial cells express type I-type II keratin pairs, and K7, K8 (type II) and K18, K19 and K20 (type I) are the primary keratins found in the single-layered intestinal epithelium. Keratins are upregulated during stress in liver, pancreas, lung, kidney and skin, however, little is known about their dynamics in the intestinal stress response. Here, keratin mRNA, protein and phosphorylation levels were studied in response to murine colonic stresses modeling human conditions, and in colorectal cancer HT29 cells. Dextran sulphate sodium (DSS)-colitis was used as a model for intestinal inflammatory stress, which elicited a strong upregulation and widened crypt distribution of K7 and K20. K8 levels were slightly downregulated in acute DSS, while stress-responsive K8 serine-74 phosphorylation (K8 pS74) was increased. By eliminating colonic microflora using antibiotics, K8 pS74 in proliferating cells was significantly increased, together with an upregulation of K8 and K19. In the aging mouse colon, most colonic keratins were upregulated. In vitro, K8, K19 and K8 pS74 levels were increased in response to lipopolysaccharide (LPS)-induced inflammation in HT29 cells. In conclusion, intestinal keratins are differentially and dynamically upregulated and post-translationally modified during stress and recovery.</p

    The amount of keratins matters for stress protection of the colonic epithelium

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    Keratins (K) are important for epithelial stress protection as evidenced by keratin mutations predisposing to human liver diseases and possibly inflammatory bowel diseases. A role for K8 in the colon is supported by the ulcerative colitis-phenotype with epithelial hyperproliferation and abnormal ion transport in K8-knockout (K8-/-) mice. The heterozygote knockout (K8+/-) colon appears normal but displays a partial ion transport-defect. Characterizing the colonic phenotype we show that K8+/- colon expresses ~50% less keratins compared to K8 wild type (K8+/+) but de novo K7 expression is observed in the top-most cells of the K8+/- and K8-/- crypts. The K8+/- colonic crypts are significantly longer due to increased epithelial hyperproliferation, but display no defects in apoptosis or inflammation in contrast to K8-/-. When exposed to colitis using the dextran sulphate sodium-model, K8+/- mice showed higher disease sensitivity and delayed recovery compared to K8+/+ littermates. Therefore, the K8+/- mild colonic phenotype correlates with decreased keratin levels and increased sensitivity to experimental colitis, suggesting that a sufficient amount of keratin is needed for efficient stress protection in the colonic epithelia
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