BACKGROUND:Drusen-like lesions beneath the retina in patients with partial lipodystrophy and type II mesangiocapillary glomerulonephritis (MCGN) were first reported in 1989. This study reports the long-term follow-up of this original cohort of patients more than 10 years later.METHODS:Three patients had undergone renal transplantation. Retinopathy was graded semiquantitatively using an international classification and grading system. Progression was assessed by comparing the visual acuities and the colour, red-free and fluorescein angiographic photographs at baseline and review.RESULTS:The visual acuity in all four patients was unchanged, as were the bilateral drusen-like lesions. The retinal pigment hypertrophy at the posterior pole of two of the patients was also unchanged. There were no signs of choroidal neovascularisation or central serous retinopathy in any patient. There was no progression of retinopathy over 10 years in any patient.CONCLUSION:This study suggests that in patients with type II MCGN, (a) factors other than drusen may contribute to choroidal neovascularisation and (b) renal transplantation does not appear to increase the risk of progression of retinopathy.

Acta Ophthalmologica ScandinavicaVolume 85, Issue s240 p. 0-0 Free Access Exenteration enucleation and evisceration: trends and dilemmas in pathology RE BONSHEK, RE BONSHEK Royal Eye Hospital, ManchesterSearch for more papers by this author RE BONSHEK, RE BONSHEK Royal Eye Hospital, ManchesterSearch for more papers by this author First published: 02 October 2007 https://doi.org/10.1111/j.1600-0420.2007.01063_2963.xAbout ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume85, Issues240September 2007Pages 0-0 RelatedInformation

Before the Court of Appeal Over three weeks in June 2005, the Court of Appeal in London heard four appeals against convictions for non-accidental injury of infants: one murder, two manslaughter, and one grievous bodily harm. The three appeal judges delivered their judgement in a 67 page document on 21 July.1 Two appeals were upheld on the grounds of process, not medical evidence, one was dismissed, and in the fourth the conviction was reduced from murder to manslaughter. The basis of the appeals was that since these convictions in the 1990s and 2000, new research had suggested that the long held belief that infants who presented with encephalopathy, thin subdural haemorrhages, and retinal haemorrhages—the triad indicating “shaken baby syndrome”—had been subjected to extreme and repeated violence was wrong and that little or no trauma need be involved. The research in question has become variously known since its publication in 2003 as the “Geddes hypothesis” or the “unified hypothesis”.2 It was based on a pathological study of the dura of 50 intra-uterine, neonatal, or infant deaths, which identified microscopic haemorrhage within the layers of the dura in 36. This led to the speculation that subdural and retinal haemorrhage was not caused by traumatic shearing of subdural veins and retinal vessels but by a combination of cerebral hypoxia, raised intra-cranial pressure from brain swelling, raised arterial pressure, and raised central venous pressure. The publication of this research was met with considerable scepticism by most working in the field of paediatrics, paediatric pathology, and paediatric head injury,3–7 but it was enthusiastically embraced by a few8, …

Inflicted head injury to the developing brain frequently results in serious disability. The pathogenesis of the neuraxial and ocular findings in infants believed to have suffered inflicted head injury remains the subject of considerable debate. Recent neuropathology studies of fatal cases of inflicted head injury and of a foetal/perinatal non-traumatic model have led to the proposal that there is a 'unified hypothesis', the essential feature of which is hypoxic brain swelling secondary to cervicomedullary injury. It has been suggested that less than violent forces may be involved and even that some cases may not be due to trauma at all. The purpose of this paper is to provide a critical review of the data upon which these suppositions are based on a background of what is already known. It is submitted that there are serious flaws in the methodology; the conclusions reached cannot logically be drawn from the data; and the 'unified hypothesis' is not supported by the evidence. On the basis of the data presented, it is also difficult to sustain the secondary hypothesis purporting to describe a minority cohort with 'infantile encephalopathy with subdural and retinal bleeding' of non-traumatic causation.

Purpose To analyse high-molecular-weight matrix glycoproteins in trabecular meshwork, cornea and sclera using SDS/PAGE and immuno- and lectin blotting. Method Extracts of normal trabecular meshwork (TM), cornea and sclera were analysed under reducing conditions on SDS/ PAGE. Western blots were stained for total protein, and major high-molecular-weight components were identified by immunoblotting with antibodies to fibronectin (FN) and type VI collagen. Lectin blotting with PSA, MPA and DSA identified some of the glycoprotein glycans. Results FN antibody bound to the 240 kDa band in TM, cornea and sclera. Type VI collagen antibody bound more strongly to one band and less so to two other bands at ~200 kDa in normal TM and to a ladder of bands in cornea and sclera. PSA and DSA bound at 240, 200 and 140 kDa in TM, cornea and sclera. MPA bound at 240, 200 and 140 kDa in TM and at 240, 200 and ~120 kDA in cornea and sclera. Conclusions FN is a component of the band at 240 kDA in TM, cornea and sclera. Normal TM was found to contain relatively more of one of the isoforms of the α3 (VI) chain whilst cornea and sclera contained all the α3 (VI) isoforms. Complex N-linked bi/tri-antennary glycans were localised in FN and the α1, α2 and α3 (VI) chains in TM, cornea and sclera. O-linked glycans (identified by MPA binding) were located in FN and α3 (VI) chains of TM, cornea and sclera.

Purpose To examine pseudophakic/aphakic bullous keratopathy (PBK/ABK) human corneas for patterns of expression of tenascin-cytotactin (TN-C) variants known to mediate specific cellular functions, viz. anti-adhesion (high molecular mass (Mr)) and adhesion (low/intermediate Mr). Methods PBK/ABK corneas were selected to encompass only those with bullae and without inflammation, scarring or neovascularisation. Serial sections from these and normal corneas were labelled with antibodies BC-4 (recognising all TN-C variants) and BC-2 (specific for the high Mr TN-C variant). Bound antibody was revealed with an avidin-biotin peroxidase technique. In a given pair of corneal sections, positivity with BC-4 but not BC-2 indicates localisation of low/intermediate Mr TN-C variants and absence of the high Mr TN-C variant. BC-2 identifies the high Mr variant. Results There was no immunostaining with either BC-2 or BC-4 in normal corneas except at the corneoscleral interface, where both BC-2 and BC-4 were immunolocalised. In PBK/ABK corneas, BC-2 staining was seen in 5 of 13 corneas and was restricted mainly to epithelial basement membrane (BM) overlying bullae. BC-2 did not label the stroma. BC-4 immunostaining was present in all PBK/ABK corneas and was localised in epithelial BM, both epithelial and stromal borders of bullae, pannus, endothelial BM and in oedematous stromal regions. Conclusions TN-C variants are differentially expressed in PBK/ABK corneas. The high Mr variant is restricted mainly to epithelial BM overlying bullae, while low/intermediate Mr variants occur in epithelial BM, both epithelial and stromal borders of bullae, and in pannus. Given the in vitro functions of TN-C, a role for promoting epithelial dehiscence and re-attachment to the substratum in PBK/ABK corneas by high and low/intermediate Mr variants respectively is likely.

CytopathologyVolume 8, Issue 6 p. 363-365 Diagnostic ophthalmic cytopathology—past, present and future R. E. BONSHEK, Corresponding Author R. E. BONSHEK Department of Histopathology/Cytopathology, Central Manchester Healthcare NHS Trust, Manchester, UKDr R. E. Bonshek, Department of Histopathology/Cytopathology, Central Manchester Healthcare NHS Trust, Clinical Sciences Building, Oxford Road, Manchester M13 9WL, UK.Search for more papers by this author R. E. BONSHEK, Corresponding Author R. E. BONSHEK Department of Histopathology/Cytopathology, Central Manchester Healthcare NHS Trust, Manchester, UKDr R. E. Bonshek, Department of Histopathology/Cytopathology, Central Manchester Healthcare NHS Trust, Clinical Sciences Building, Oxford Road, Manchester M13 9WL, UK.Search for more papers by this author First published: 24 May 2007 https://doi.org/10.1111/j.1365-2303.1997.tb00565.xCitations: 2AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Citing Literature Volume8, Issue6December 1997Pages 363-365 RelatedInformation

Twelve specimens of resin-embedded human trabecular meshwork were probed with a panel of 21 biotinylated lectins, using an avidin-biotin peroxidase revealing system, in order to determine the normal pattern of saccharide expression in this tissue. High-mannose, intermediate and hybrid N-linked glycans, and complex N-linked bisected and non-bisected bi/tri-antennate glycans, as shown by the binding of Canavalia ensiformis (ConA), Pisum sativum (PSA), Lens culinaris (LCA) agglutinins and Phaseolus vulgaris erythroagglutinin (ePHA), were strongly expressed by the canal of Schlemm endothelium and juxtacanalicular tissue, but less so by the corneoscleral meshwork. Highly branched complex glycans were not found, as there was no binding by Phaseolus vulgaris leukoagglutinin (1PHA). Sialyl residues, especially those α2,6-linked as demonstrated by strong Sambucus nigra (SNA) lectin staining, were also abundant in this area. N-acetyllactosamine sequences and some O-linked glycans were present in the trabecular meshwork, as shown by Solanum tuberosum (STA), Datura stramonium (DSA), and Jacalin (Jac) lectin binding, while fucose residues were not detected by Tetragonolobus purpureas (LTA) or Ulex europaeus-1 (UEA-1) agglutinins. These results indicate similarities with renal glomerular and vascular endothelium, although the lack of binding with UEA-1 agglutinin suggests differences which may relate to the specialized function of the trabecular meshwork. This study provides a baseline for comparative analysis of the glycans of human trabecular meshwork in pathological conditions such as primary open-angle glaucoma.

normal bilaterally. The right upper eyelid was ptotic (Fig la). No eyelid retraction was noted on opening the jaw or moving it to the left side. The right upper eyelid elevated on clenching the teeth (Fig lb). The levator functions were normal bilaterally. The pupils were isocoric, and pupillary light reactions were prompt bilaterally. Both eyes appeared otherwise normal. Electroencephalography and computed tomography of the brain and orbits showed normal findings.

A panel of 14 lectins was used to investigate the expression of saccharides by cerebral microvessels (MBV) in ageing, Alzheimer's disease (AD) and Down's syndrome (DS). Broad increases in lectin binding with age may reflect changes in amount and diversity of glycoproteins due to the thickening of the basement membrane (BM) common in older persons. In AD, and in persons over 50 years of age with DS, binding of e-PHA, 1-PHA and PAA was increased beyond that of age alone, as was that of UEA-I and BSA-1B4 in AD, but not in DS. Persons under 50 years of age with DS showed no changes inappropriate to their age. These specific increases in AD and DS may reflect selective disease-related changes in BM and could indicate an impaired blood-brain barrier (bbb) function or integrity. However, because they occur (in DS) after the deposition of amyloid (A4) protein and onset of neurofibrillary degeneration, it is unlikely they induce plaque and tangle formation. Such changes in MBV could stem from the loss of neurones from locus caeruleus, raphe and nucleus basalis (which are thought to innervate MBV and exert control over blood flow and permeability) that occurs in DS after 50 years of age.

A monoclonal antibody, M2, was produced by somatic cell hybridisation of splenocytes, from mice immunised with human fetal brain, with the murine myeloma cell line NS-1. Indirect immuno-peroxidase staining of formalin-fixed, paraffin embedded tissue sections showed that, whilst the monoclonal antibody gave a positive reaction with 32/39 astrocytomas from adult patients and 33/36 of children's astrocytomas of the adult histological type, only 17/39 of juvenile astrocytomas were stained. A Chi-squared test showed that the difference in staining between the two groups (adult versus juvenile) was highly significant (p less than 0.0001). In contrast, using a polyclonal antiserum to GFAP, a significantly larger proportion of juvenile astrocytomas than adult astrocytomas stained positively (p less than 0.05). Thus, whereas the distribution of GFAP accorded with the general finding that the degree of malignancy of a tumour correlates with the loss of cell type specific markers, the distribution of M2 reactivity was similar to that of some oncogene products which increase with malignancy. From the flow cytometry data it is apparent that the antigen recognised by M2 is not cell cycle dependent.