Relationship of "bleeding on probing" and "gingival index bleeding" as clinical parameters of gingival inflammation

Abstract Bleeding on probing (BOP) and the gingival index have been used to clinically characterize the degree of gingival inflammation. It is, however, unclear to what extent these parameters correlate to each other and to probing pocket depth (PD). The purpose of this clinical study was to evaluate the association between BOP and GI bleeding (scores of 2 and 3), as well as the relationship of these variables to PD, in a group of patients presenting with naturally-occurring gingivitis. Based on screening examinations of 125 subjects with at least 20 teeth, no more than 4 sites with PD over 6 mm, a BOP frequency of 30% or greater, and no systemic condition that would influence the inflammatory response, were selected. 2 weeks after screening they were examined at 6 sites per tooth for plaque index, GI, PD and BOP. A standardized pressure sensitive probe (Florida Probe) with 20 g probing force was used for BOP and PD measurements. In this population, means of 40.9% (S.E.= 1.36) BOP sites and 35.3% (S.E, = 1.81) GI bleeding sites per patient were found. A total of 20,008 sites ranging in PD up to 5.9 mm were evaluated; however, the majority of sites (19,723, 98.6%) presented with <4 mm PD. When sites were evaluated, BOP demonstrated a positive correlation with PD, whereas GI bleeding correlated with PH. For sites characterized by the absence of BOP as well as the absence of GI bleeding (scores 0 and 1), the highest % of agreement between the 2 indices (77.7%) was found in shallow sites (0.1–2 mm). In contrast, when sites presenting with both BOP and GI bleeding were analyzed, the highest % of agreement (85,4%) was found for sites with PD >4.0 mm. In this gingivitis population group, it appears that BOP and GI bleeding evaluate distinct inflammatory1 conditions of the gingival tissues, and the relationship between the 2 clinical parameters may vary according to PD at the individual site examined.     

FEASIBILITY OF CONDUCTING CARDIOVASCULAR OUTCOME RESEARCH IN AUSTRALIAN GENERAL PRACTICE: RESULTS FROM THE ANBP2 PILOT STUDY

1. The present study aimed to determine the feasibility of conducting a 5 year cardiovascular outcome trial of the treatment of 6000 elderly hypertensive patients in Australian general practices. 2. General practitioners (GPs) were invited to participate by mail and personal follow-up. Patient records were reviewed to identify subjects for a blood pressure (BP) screening programme. Blood pressure was measured on three occasions and eligible subjects were included if the average BP was 160 mmHg systolic or 90 mmHg diastolic if systolic BP was 140 mmHg. 3. Seven hundred and forty-one GPs were approached and 89 were enrolled in the study (12% of mail invites and 75% of those receiving a personal contact). In 16 practices where screening was completed, 82 000 records were reviewed to identify 4% patients eligible for screening. Twenty-two per cent of eligible subjects attended screening. Of 1938 subjects screened, 180 (9%) had BP 5=160/90 mmHg. Forty-seven percent of subjects (n = 916) were receiving antihypertensive therapy and 184 (20%) were withdrawn from therapy. One hundred and sixteen (63%) of these subjects had BP return to study entry levels within 6 weeks. Fifty-seven newly diagnosed and 81 previously treated subjects were randomized (7% of the screened population). 4. Based on the high participation rate of GPs, the response rate of patients to attend a BP screening programme and the 7% randomization to screening ratio for entry into the study, the ANBP2 pilot study has demonstrated that it is feasible to recruit subjects from Australian general practices to a cardiovascular outcome trial.     

Ontogeny of peroxidase activity in epithelium and eosinophils of the mouse uterus.

Outbred CD-1 mice treated for 1 or 4 days with 1 mg/kg of diethylstilbestrol (DES) at various ages after birth were examined for histochemical localization of peroxidase in the uterine epithelium. Peroxidase activity in uterine extracts was also measured by a radiometric assay and the conversion of [3H]DES to [3H]Z,Z-diensestrol (Z,Z-DIES). While no peroxidase activity was detected by a histochemical method in uterine epithelium from untreated 5-day old mice, the enzyme was apparent in mice treated for 4 days with DES; uterine eosinophils were absent at this age. By day 9, DES-induced staining for peroxidase in uterine epithelial cells and the number of uterine eosinophils had increased significantly. In addition, at this age, the biochemical assays for uterine peroxidase were sensitive enough to show that DES is converted to Z,Z-DIES and that [3H]estradiol gives rise to 3H2O and water-soluble radioactive metabolites. The peroxidase response to DES, determined by both histochemical and biochemical methods, increased with the age of the immature mice. These data indicate that the neonatal uterus, although deficient in eosinophils, demonstrates a peroxidase response to estrogen and that this response is localized primarily in the luminal epithelium. The role of this DES-induced peroxidase activity in converting DES to activated metabolites that may cause cell damage is discussed.     

肌病肾病代谢综合征治疗进展

肌病肾病代谢综合征是急性动脉阻塞致骨骼肌溶解的严重并发症。积极治疗原发病，及早补液扩容、碱化尿液、早期血液净化治疗是降低截肢率、病死率的关键。本文就肌病肾病代谢综合征治疗进展作一综述。     

单独肝尾状叶血管瘤切除术

肝尾状叶由于解剖位置特殊,位置深,难以显露,手术难度大,是肝脏外科领域手术操作的难点与研究热点.随着肝血流控制技术的发展、肝实质离断技术的提高,肝尾状叶肿瘤切除率明显提高[1].2006年4月至2008年10月,我科完成单独肝尾状叶血管瘤切除术9例,现将手术技巧与疗效报道如下.     

An Immunohistochemical Study of the Pathology of Fatal Malaria: Evidence for Widespread Endothelial Activation and a Potential Role for Intercellular Adhesion Molecule-1 in Cerebral Sequestration

The sequestration of parasitized erythrocytes in the microvasculature of vital organs is central to the pathogenesis of severe Plasmodium falciparum malaria. This process is mediated by specific interactions between parasite adherence ligands and host receptors on vascular endothelium such as intercellular adhesion molecule-1 (ICAM-1) and CD36. Using immunohistochemistry we have examined the distribution of putative sequestration receptors in different organs from fatal cases of P.falciparum malaria and noninfected controls. Receptor expression and parasite sequestration in the brain were quantified and correlated. Fatal malaria was associated with widespread induction of endothelial activation markers, with significantly higher levels of ICAM-1 and E-selectin expression on vessels in the brain. In contrast, cerebral endothelial CD36 and thrombospondin staining were sparse, with no evidence for increased expression in malaria. There was highly significant co-localization of sequestration with the expression of ICAM-1, CD36, and E-selectin in cerebral vessels but no cellular inflammatory response. These results suggest that these receptors have a role in sequestration in vivo and indicate that systemic endothelial activation is a feature of fatal malaria.     

Plasmodium falciparum rosetting is associated with malaria severity in Kenya.

Rosette formation in 154 fresh Plasmodium falciparum isolates from Kenyan children with mild (n = 54), moderate (n = 64), or severe (n = 36) malaria was studied to determine whether the ability to form rosettes in vitro is correlated with malaria severity. There was a wide distribution of rosette frequencies within each clinical category; however, a clear trend towards higher rosette frequency with increasing severity of disease was seen, with the median rosette frequency of the mild-malaria group (1%; range, 0 to 82%) being significantly lower than those of the moderate-malaria group (5%; range, 0 to 45%; Mann-Whitney U test, P < 0.02) and the severe-malaria group (7%; range, 0 to 97%; Mann-Whitney U test, P < 0.003). Within the severe-malaria category there was no difference in rosetting among isolates from cerebral malaria patients or those with other forms of severe malaria. We also examined the ABO blood groups of the patients from whom isolates were obtained and found that isolates from group O patients (median rosette frequency, 2%; range 0 to 45%) rosetted less well than those from group A (median, 7%; range 0 to 82%; Mann-Whitney U test, P < 0.01) or group AB (median, 11%; range 0 to 94%; Mann-Whitney U test, P < 0.03). We therefore confirm that rosetting is associated with severe malaria and provide further evidence that rosetting is influenced by ABO blood group type. Whether rosetting itself plays a direct role in the pathogenesis of severe malaria or is a marker for some other causal factor remains unknown.     

Microarray-based comparative genomic analyses of the human malaria parasite Plasmodium falciparum using Affymetrix arrays

Microarray-based comparative genomic hybridization (CGH) provides a powerful tool for whole genome analyses and the rapid detection of genomic variation that underlies virulence and disease. In the field of Plasmodium research, many of the parasite genomes that one might wish to study in a high throughput manner are not laboratory clones, but clinical isolates. One of the key limitations to the use of clinical samples in CGH, however, is the miniscule amounts of genomic DNA available. Here we describe the successful application of multiple displacement amplification (MDA), a non-PCR-based amplification method that exhibits clear advantages over all other currently available methods. Using MDA, CGH was performed on a panel of NF54 and IT/FCR3 clones, identifying previously published deletions on chromosomes 2 and 9 as well as polymorphism in genes associated with disease pathology.     

Vascular networks of the nucleus lentiformis

Summary The nucleus lentiformis vascular networks were studied in 30 brains by injecting the vascular system with gelatinous Indian ink. The nucleus lentiformis is divided into a medial part, the globus pallidus, and a lateral part, the putamen. These two parts differ completely from one another in their embryology, structure and functions. For these reasons, each part presents a specific vascular network. The putaminal network is dense and shows many similarities with the cerebral cortex vascular network; the pallidal one is simpler and less dense. These two vascular networks are located close to each other without overlapping. Their specificity may be in relation with the histological structure, with the morphogenetic evolution or with the functional activity of both nuclei to which they provide the vascularization.

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Les réseaux vascularies du noyau lenticulaire

Résumé L'étude des réseaux vasculaires du noyau lenticulaire (NL) est réalisée sur 30 cerveaux dont le système vasculaire a été injecté à l'encre de Chine gélosée. Le NL est constitué par deux parties, le putamen (néostriatum) et le globus pallidus (paléo-striatum), totalement différentes sur les plans morphologique, embryologique et fonctionnel. Chacune de ces parties possède un réseau vasculaire spécifique et caractéristique. Les deux réseaux se côtoient sans se chevaucher. Le réseau vasculaire putaminal est dense et présente de nombreuses similitudes avec le réseau vasculaire du cortex cérébral. Le réseau vasculaire pallidal se caractérise par sa simplicité et sa moindre densité. Leur spécificité peut être en rapport avec la structure histologique, l'évolution morphogénétique et avec l'activité fonctionnelle des noyaux dont ils assurent l'irrigation.

     

Functional characterization of missense mutations at codon 838 in retinal guanylate cyclase correlates with disease severity in patients with autosomal dominant cone-rod dystrophy

Three different mutations in codon 838 of GUCY2D, the gene for retinal guanylate cyclase 1, have been linked to autosomal dominant cone-rod dystrophy at the CORD6 locus. To examine the relationship between enzyme activity and disease severity, the three disease-causing substitutions (R838C, R838H and R838S) and four artificial mutations (R838A, R838E, R838L and R838K) were generated. Assay of GCAP1-stimulated cyclase activity in vitro shows that, compared with wild-type, R838E, R838L and R838K possess only low activity, whereas R838A, R838C, R838H and R838S have activity equal or superior to wild-type at low Ca(2+) concentrations. These four latter mutants showed a higher apparent affinity for GCAP1 than did wild-type. The Ca(2+) sensitivity of the GCAP1 activation was also altered with marked residual activity at high Ca(2+), the effect increasing: wild-type < R838C < R838H < R838A < R838S. Within the photoreceptor, this would result in a failure to inactivate cyclase activity at high physiological Ca(2+ )concentrations. Amongst the three disease-associated mutations, the effect correlates directly with disease severity. The wild-type and R838H mutant displayed a difference in pH sensitivity, with the mutant showing a higher specific activity with pH > 6.0. Site 838 is in the dimerization domain that forms a coiled-coil in the active protein. A computer-aided structure prediction of this region indicates that R838 in the wild-type breaks the structure at four helical turns, and there is an increasing tendency for the structure to continue for further turns in the order R838C < R838H,S,K < R838E < R838A < R838L.