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Biomedical subjects

S Mallory

Publications and source records attributed to S Mallory.

8 recordsLinked to original sources
PubMed2004

Anaesthetic management in facial bipartition surgery: the experience of one centre.

Facial bipartition is amongst the most radical craniofacial surgery undertaken but is performed rarely. There is little published information on its anaesthetic management. We undertook a retrospective case-note review of 22 consecutive patients undergoing bipartition surgery by the same surgical team in one centre in the period 1993-2001. There were incomplete data for two cases and these were therefore excluded. Patients were aged 2 months to 19 years. Conditions treated were facial cleft (n = 5), frontonasal dysplasia (n = 7) and facial dysostosis (n = 8).Intra-operative complications included major haemorrhage (n = 4), bradycardia (n = 3) and unintentional tracheal extubation (n = 1). There were no peri-operative deaths. All patients required intra-operative blood transfusion and 15% of them had a postoperative haemoglobin concentration > 115% of their pre-operative value. In this series, four patients required postoperative lung ventilation for a median duration of 3 days. Infants < 14 months old were significantly more likely to receive a massive blood transfusion (p = 0.0002), to have an excessively high postoperative haematocrit (p = 0.008) and to require postoperative lung ventilation (p = 0.0002) compared with older patients. We conclude that patients in this age group have a significantly increased risk of postoperative complications.

Adolescent↗
PubMed2004

Extending low-dose epidural analgesia for emergency Caesarean section using ropivacaine 0.75%.

We compared ropivacaine 0.75% and bupivacaine 0.5% for extending low-dose epidural analgesia for emergency Caesarean section, using a prospective double-blind randomised controlled trial design. The trial was halted after 45 patients were studied (23 ropivacaine; 22 bupivacaine) because bupivacaine was replaced by levobupivacaine in our unit. Time to reach T4 for loss of cold sensation was similar in both groups, although analgesic supplementation was required less often in the ropivacaine group than in the bupivacaine group (2/23 vs. 9/21; p = 0.01).

Adult↗
PubMed2001

12-year-old male with Elejalde syndrome (neuroectodermal melanolysosomal disease).

Neuroectodermal melanolysosomal disease, also known as Elejalde syndrome, is a rare syndrome characterized by silvery hair, pigment abnormalities, and profound central nervous system dysfunction. It is similar to the Chediak-Higashi and Griscelli syndromes, although these syndromes are associated with severe immunologic dysfunction. We report on a 12-year-old male with Elejalde syndrome and compare the Elejalde, Chediak-Higashi, and Griscelli syndromes.

Adolescent↗
PubMed2001

Essential role played by the C-terminal domain of glycoprotein I in envelopment of varicella-zoster virus in the trans-Golgi network: interactions of glycoproteins with tegument.

Varicella-zoster virus (VZV) is enveloped in the trans-Golgi network (TGN). Here we report that glycoprotein I (gI) is required within the TGN for VZV envelopment. Enveloping membranous TGN cisternae were microscopically identified in cells infected with intact VZV. These sacs curved around, and ultimately enclosed, nucleocapsids. Tegument coated the concave face of these sacs, which formed the viral envelope, but the convex surface was tegument-free. TGN cisternae of cells infected with VZV mutants lacking gI (gI(Delta)) or its C (gI(DeltaC))- or N-terminal (gI(DeltaN))-terminal domains were uniformly tegument coated and adhered to one another, forming bizarre membranous stacks. Viral envelopment was compromised, and no virions were delivered to post-Golgi structures. The TGN was not gI-immunoreactive in cells infected with the gI(Delta) or gI(DeltaN) mutants, but it was in cells infected with gI(DeltaC) (because the ectodomains of gI and gE interact). The presence in the TGN of gI lacking a C-terminal domain, therefore, was not sufficient to maintain enveloping cisternae. In cells infected with intact VZV or with gI(Delta), gI(DeltaN), or gI(DeltaC) mutants, ORF10p immunoreactivity was concentrated on the cytosolic face of TGN membranes, suggesting that it interacts with the cytosolic domains of glycoproteins. Because of the gE-gI interaction, cotransfected cells that expressed gE or gI were able to target truncated forms of the other to the TGN. Our data suggest that the C-terminal domain of gI is required to segregate viral and cellular proteins in enveloping TGN cisternae.

Animals↗
PubMed1998

Analysis of the glycoproteins I and E of varicella-zoster virus (VZV) using deletional mutations of VZV cosmids.

The contributions of the glycoproteins gI (ORF67) and gE (ORF68) to varicella-zoster virus (VZV) replication were investigated in deletion mutants made by using cosmids with VZV DNA derived from the Oka strain. These experiments demonstrated that gI was not required for VZV replication in vitro but gE appeared to be. Although VZV gI was not required, its deletion or mutation resulted in a significant decrease in infectious virus yields, and it disrupted syncytial formation and altered the conformation and distribution of gE in infected cells. Normal cell-to-cell spread and replication kinetics were restored when gI was expressed from a non-native locus in the VZV genome. The expression of intact gI, the ORF67 gene product, is required for efficient VZV replication.

Cell Line↗
PubMed1997

Mutational analysis of the role of glycoprotein I in varicella-zoster virus replication and its effects on glycoprotein E conformation and trafficking.

The contributions of the glycoproteins gI (ORF67) and gE (ORF68) to varicella-zoster virus (VZV) replication were investigated in deletion mutants made by using cosmids with VZV DNA derived from the Oka strain. Deletion of both gI and gE prevented virus replication. Complete deletion of gI or deletions of 60% of the N terminus or 40% of the C terminus of gI resulted in a small plaque phenotype as well as reduced yields of infectious virus. Melanoma cells infected with gI deletion mutants formed abnormal polykaryocytes with a disrupted organization of nuclei. In the absence of intact gI, gE became localized in patches on the cell membrane, as demonstrated by confocal microscopy. A truncated N-terminal form of gI was transported to the cell surface, but its expression did not restore plaque morphology or infectivity. The fusogenic function of gH did not compensate for gI deletion or the associated disruption of the gE-gI complex. These experiments demonstrated that gI was dispensable for VZV replication in vitro, whereas gE appeared to be required. Although VZV gI was dispensable, its deletion or mutation resulted in a significant decrease in infectious virus yields, disrupted syncytium formation, and altered the conformation and distribution of gE in infected cells. Normal cell-to-cell spread and replication kinetics were restored when gI was expressed from a nonnative locus in the VZV genome. The expression of intact gI, the ORF67 gene product, is required for efficient membrane fusion during VZV replication.

Biological Transport↗
PubMed1986

Congenital herpes simplex retinitis.

An 1,810-g girl born at 37 weeks of gestation had true congenital herpes simplex virus type 2 infection. The neonate was born with hypo-pigmented skin lesions, brain lesions, and old heavily pigmented retinal scars in the posterior pole. There was no active ocular disease. Viral cultures, immunoperoxidase stains, and antibody determination by enzyme-linked immunosorbent assay were all positive for herpes simplex virus. Treatment with acyclovir healed the lesions within ten days. The clinical and laboratory findings indicated that the herpetic infection probably occurred in the second trimester.

Female↗