Comparative fluorescence spectroscopy of root caries lesions

In this study, the light-emission properties of carious and sound root surfaces were investigated under a wide range of excitation wavelengths. Human molar teeth with exposed root surfaces containing light- and dark-discolored root caries (n = 3 of each) were selected. Emission spectra were recorded from carious and corresponding sound root surface areas from each tooth by using a fluorescence spectrophotometer at excitation wavelengths from 360 nm up to 580 nm, in steps of 20 nm. The spectra were corrected for fluctuations in detector sensitivity and excitation light intensity, and normalized to peak intensity. Excitation spectra were recorded for selected emission wavelengths that showed maximum intensity. Light- and dark-discolored root surface caries showed distinct fluorescence emission bands between 600 and 700 nm that were not present in sound root surface areas. These bands were strongest for excitation wavelengths between 390 and 420 nm. The excitation spectra of root caries revealed maximum excitation at around 405 nm, which is equivalent to the Soret band of porphyrin compounds. The emission spectra of both types of root caries lesions were shifted towards longer wavelengths (red shift at half maximum) when compared to the spectra of corresponding sound root surfaces. The red shift for dark-discolored root caries was higher than for light-discolored lesions at all excitation wavelengths.     

Discoid lupus erythematosus

Discoid lupus erythematosus is a manifestation of chronic cutaneous lupus erythematosus with a small risk of systemic involvement. In this review article, the role of predisposing factors such as haplotype, hormones, antibodies and sunlight are discussed. The clinical features, including variants and associations, and management options are presented.     

Elective percutaneous coronary intervention without on-site cardiac surgery: clinical and economic implications

BACKGROUND: Low procedural complication rates, barriers to access, and patient preference have encouraged the development of percutaneous coronary intervention (PCI) programs at centers that are often closer to home but without on-site cardiac surgical capability. OBJECTIVES: We compared clinical and economic outcomes associated with performing low-risk elective PCI at a community hospital without on-site cardiac surgery with those obtained at a more remote tertiary care center with on-site cardiac surgery. DESIGN AND MEASURES: We matched 257 patients undergoing low-risk, elective PCI at a community hospital (Immanuel St. Joseph's Hospital [ISJ] between January 27, 2000, and July 31, 2002) to 514 PCI patients treated at a tertiary care hospital (Saint Marys Hospital [SMH] between January 27, 2000, and April 30, 2002) based on clinical and lesion criteria. Clinical outcomes (in-hospital procedural success and target vessel failure during long-term follow up) and economic outcomes (direct medical costs, billed charges, and hospital length of stay [LOS]) were compared between groups. The Mayo Clinic PCI Registry (containing clinical, angiographic, and follow-up data) and administrative data were used in matching and outcomes assessment. RESULTS: Procedural success was achieved more often among ISJ-treated patients (99% vs. 95%; P = 0.02); however, no difference in target vessel failure rates was observed during a median follow-up time of 3.1 years (estimated 1-year event rate: 15.2% vs. 14.8%; P = 0.46). ISJ-treated patients incurred, on average, $3024 more in estimated total costs ($13,771 vs. $10,746; P < 0.001) and $6084 more in billed charges (P < 0.001), but incurred similar LOS post procedure (1.53 days). CONCLUSIONS: Similar clinical outcomes were achieved at a community hospital without on-site cardiac surgery but at significantly increased direct medical cost. Patients, providers, hospitals, payers, and policymakers should consider whether the benefits associated with locally provided specialized cardiovascular services warrant this additional cost.     

Gastrointestinal hypomotility with loss of enteric nicotinic acetylcholine receptors: active immunization model in mice

Background Autoimmune gastrointestinal dysmotility (AGID) is a limited form of dysautonomia. The only proven effector to date is IgG specific for ganglionic nicotinic‐acetylcholine receptors containing α3 subunits [α3*‐ nicotinic acetylcholine receptor (nAChR)]. Rabbits immunized with recombinant α3‐polypeptide produce α3*‐nAChR autoantibodies, and profound AGID ensues. Human and rabbit α3*‐nAChR‐specific‐IgGs induce transient hypomotility when injected into mice. Here, we describe success and problems encountered inducing gastrointestinal hypomotility in mice by active immunization. Methods We repeatedly injected young adult mice of seven different strains susceptible to autoimmunity (spontaneous diabetes or neural antigen immunization‐induced myasthenia gravis or encephalomyelitis) with: (i) α3‐polypeptide, intradermally or (ii) live α3*‐nAChR‐expressing xenogeneic cells, intraperitoneally. We measured serum α3*‐nAChR‐IgG twice monthly, and terminally assessed blue dye gastrointestinal transit, total small intestinal α3*‐nAChR content (radiochemically) and myenteric plexus neuron numbers (immunohistochemically, ileal–jejunal whole‐mount preparations). Key Results Standard cutaneous inoculation with α3‐polypeptide was minimally immunogenic, regardless of dose. Intraperitoneally injected live cells were potently immunogenic. Self‐reactive α3*‐nAChR‐IgG was induced only by rodent immunogen; small intestinal transit slowing and enteric α3*‐nAChR loss required high serum levels. Ganglionic neurons were not lost. Conclusions & Inferences Autoimmune gastrointestinal dysmotility is inducible in mice by active immunization. Accompanying enteric α3*‐nAChR reduction without neuronal death is consistent with an IgG‐mediated rather than T cell‐mediated pathogenesis, as is improvement of symptoms in patients receiving antibody‐depleting therapies.     

4种支架构建复合式口腔黏膜的组织学特点

目的利用4种不同支架材料构建复合式口腔黏膜,并比较其组织结构特点。方法体外培养人口腔黏膜的成纤维细胞和角质形成细胞,在4种支架材料中加入成纤维细胞,培养7d后,在支架表面加入角质形成细胞,培养4d后,移至气-液界面继续培养7d。苏木精-伊红染色镜下观察构建的复合式口腔黏膜的组织形态学特点。结果 4种支架均可构建形成复层上皮。其中,上皮层与脱细胞真皮基质材料(de-epidermised dermis,DED)结合紧密,形成的人工黏膜有明显的上皮钉突。不同于以往报道,上皮层与Alloderm结合并不十分紧密。以胶原凝胶为基质形成的人工口腔黏膜最厚,有明显分层。以胶原海绵-胶原凝胶为基质形成的复层上皮在部分区域长入至胶原海绵的空隙中。结论以DED和胶原凝胶为支架构建的口腔黏膜更接近于天然结构,而后者脆性较大,限制了其临床应用的可能。     

The effects of different alcoholic drinks on lipids, insulin and haemostatic and inflammatory markers in older men

Light to moderate drinking is associated with lower risk of coronary heart (CHD) than non-drinkers. We have examined the relationships between total alcohol intake and type of alcoholic beverage and several potential biological mechanisms. We carried out the study in 3158 men aged 60-79 years drawn from general practices in 24 British towns with no history of myocardial infarction, stroke or diabetes and who were not on warfarin. Total alcohol consumption showed a significant positive dose-response relationship with high density lipoprotein cholesterol (HDL-C), coagulation factor IX, haematocrit, blood viscosity, and tissue plasminogen (t-PA) antigen, and an inverse dose-response relationship with insulin, fibrinogen, von Willebrand factor (vWF) and triglycerides after adjustment for possible confounders. Total alcohol consumption showed weak associations with plasma viscosity and fibrin D-dimer, and no association with factors VII, VIII, or C-reactive protein (CRP). Wine was specifically associated with lower CRP, plasma viscosity, factor VIII and triglycerides. The findings are consistent with the suggestion that HDL-C in particular but also insulin and haemostatic factors may contribute to the beneficial effect of light to moderate drinking on risk of CHD. Wine has effects that may confer greater protection than other alcoholic beverages.     

Prospective evaluation of posttransfusion hepatitis

The incidence of posttransfusion hepatitis (PTH) was determined prospectively at our institution. An active surveillance program of transfused surgical patients was set up; alanine aminotransferase (ALT) levels were determined before transfusion and at monthly intervals for 6 months after transfusion. Patients with confirmed ALT values greater than 2.5 times the upper reference values were referred to the out-patient clinics for diagnosis. Of 4051 surgical patients who underwent transfusion between January 1986 and December 1989, 2459 (60.7%) were enrolled in the surveillance program, and 1018 (25.1%) completed the follow-up; 238 patients received autologous blood only and were used as controls. No PTH was observed in the control patients, and the incidence of the disease in patients receiving homologous blood was 10.97 percent in 1986, 6.58 percent in 1987, 5.55 percent in 1988, and 4.29 percent in 1989; the decreasing trend is significant (p = 0.018).     

A founder mutation in BBS2 is responsible for Bardet‐Biedl syndrome in the Hutterite population: utility of SNP arrays in genetically heterogeneous disorders

Innes AM, Boycott KM, Puffenberger EG, Redl D, MacDonald IM, Chudley AE, Beaulieu C, Perrier R, Gillan T, Wade A, Parboosingh JS. A founder mutation in BBS2 is responsible for Bardet‐Biedl syndrome in the Hutterite population: utility of SNP arrays in genetically heterogeneous disorders. Bardet‐Biedl syndrome (BBS) is a multisystem genetically heterogeneous disorder, the clinical features of which are largely the consequence of ciliary dysfunction. BBS is typically inherited in an autosomal recessive fashion, and mutations in at least 14 genes have been identified. Here, we report the identification of a founder mutation in the BBS2 gene as the cause for the increased incidence of this developmental disorder in the Hutterite population. To ascertain the Hutterite BBS locus, we performed a genome‐wide single nucleotide polymorphism (SNP) analysis on a single patient and his three unaffected siblings from a Hutterite family. The analysis identified two large SNP blocks that were homozygous in the patient but not in his unaffected siblings, one of these regions contained the BBS2 gene. Sequence analysis and subsequent RNA studies identified and confirmed a novel splice site mutation, c.472‐2A>G, in BBS2. This mutation was also found in homozygous form in three subsequently studied Hutterite BBS patients from two different leuts, confirming that this is a founder mutation in the Hutterite population. Further studies are required to determine the frequency of this mutation and its role, if any, in the expression of other ciliopathies in this population.