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Microscopic Appearance (microscopic + appearance)
Selected AbstractsEffect of bleaching agents on bonding to pulp chamber dentineINTERNATIONAL ENDODONTIC JOURNAL, Issue 4 2005S. Timpawat Abstract Aim, To determine the effect of intracoronal bleaching agents on adhesion of bonding agents to pulp chamber dentine. Methodology, Forty extracted human maxillary anterior teeth were randomly divided into four groups of 10 teeth each. Bleaching agents were sealed in pulp chambers for 7 days, as in clinical use. Group 1 (control): distilled water, group 2: 35% hydrogen peroxide, group 3: sodium perborate mixed with water, and group 4: sodium perborate mixed with 35% hydrogen peroxide. Teeth were stored in saline at 37 °C for 7 days. After the bleaching agent was removed, teeth were leached in water for a further 7 days prior to bonding. The crown was cut vertically from mesial to distal and the labial pulp chamber dentine was prepared for bonding with Clearfil SE-Bond and filled with resin composite (Clearfil AP-X). The bonded specimens were kept moist at 37 °C for 24 h. Microtensile bond strengths were determined using a universal testing machine. Additional teeth were prepared using the same bleaching procedures to investigate the scanning electron microscopic appearance of the dentine surface. Results, Mean values (±SD) of microtensile bond strength for the experimental groups were: group 1: 5.29 ± 2.21 MPa, group 2: 5.99 ± 1.51 MPa, group 3: 9.17 ± 1.65 MPa and group 4: 3.99 ± 1.31 MPa. Dentine treated with sodium perborate in water (group 3) had significantly higher mean bond strength when compared with the other three groups (P < 0.05, Tukey's test). Mean bond strength was lowest when dentine was treated with sodium perborate plus hydrogen peroxide (group 4). Conclusions, In terms of subsequent bond strength during restoration, sodium perborate mixed with distilled water appears to be the best intracoronal bleaching agent. [source] Juvenile psoriatic arthritis with nail psoriasis in the absence of cutaneous lesionsINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 1 2000Carola Duran-McKinster MD A 4-year-old white boy without a significant family history had morning stiffness and painful swelling of his left knee and ankle, right elbow, and dorsolumbar region of 2 months' evolution. The following laboratory studies were within normal limits: complete blood cell count, C-reactive protein (CRP), latex, antistreptolysin, and antinuclear antibodies. Rheumatoid factor was negative and an increase in the erythrocyte sedimentation rate (ESR) was detected (56 mm/h). The pediatric department made an initial diagnosis of juvenile rheumatoid arthritis, and treatment with acetylsalicylic acid at 100 mg/kg/day and naproxen at 10 mg/kg/day was started. A thick, yellowish toenail was diagnosed as onychomycosis. No mycologic investigations were performed. Intermittent episodes of painful arthritis of different joints were present. The radiographic features of the peripheral joints included: narrow joint spaces, articular erosions, soft tissue swelling, and diffuse bony demineralization. Characteristic bilateral sacroiliitis and a swollen tendon sheath on the left ankle were detected. At 11 years of age the nail changes had extended to five other toenails and to four fingernails, were yellow,brown in color, and showed marked subungual hyperkeratosis ( Figs 1, 2). The rest of the nails showed significant nail pitting. Trials of griseofulvin alternated with itraconazole in an irregular form for five consecutive years resulted in no clinical improvement, which prompted a consultation to our dermatology department. On three different occasions, KOH nail specimens were negative for fungus, but the presence of parakeratotic cells aroused the suspicion of psoriasis. A complete physical examination was negative for psoriatic skin lesions. A nail bed biopsy specimen was characteristic of nail psoriasis ( Fig. 3). Figure 1. Thickened nails with severe subungual hyperkeratosis in five fingernails Figure 2. Secondary deformity of nail plate. No "sausage" fingers were observed Figure 3. Light microscopic appearance of a nail biopsy specimen showing parakeratotic hyperkeratosis, elongation of interpapillary processes, and Munroe abscess (arrow) (hematoxylin and eosin stain, ×40) The following human leukocyte antigens (HLAs) were positive: A9, A10, B12, B27, Cw1, Bw4, DR6, DR7, DQ1, DQ2, and DR53. A diagnosis of juvenile psoriatic arthritis associated with nail psoriasis was made. Toenail involvement became so painful that walking became very difficult. Occlusive 40% urea in vaseline applied to the affected toenails for 48 h resulted in significant improvement. Currently, the patient is 20 years old with nail involvement, but no psoriatic skin lesions have ever been observed. [source] Origin of migmatites by deformation-enhanced melt infiltration of orthogneiss: a new model based on quantitative microstructural analysisJOURNAL OF METAMORPHIC GEOLOGY, Issue 1 2008P. HASALOVÁ Abstract A detailed field study reveals a gradual transition from high-grade solid-state banded orthogneiss via stromatic migmatite and schlieren migmatite to irregular, foliation-parallel bodies of nebulitic migmatite within the eastern part of the Gföhl Unit (Moldanubian domain, Bohemian Massif). The orthogneiss to nebulitic migmatite sequence is characterized by progressive destruction of well-equilibrated banded microstructure by crystallization of new interstitial phases (Kfs, Pl and Qtz) along feldspar boundaries and by resorption of relict feldspar and biotite. The grain size of all felsic phases decreases continuously, whereas the population density of new phases increases. The new phases preferentially nucleate along high-energy like,like boundaries causing the development of a regular distribution of individual phases. This evolutionary trend is accompanied by a decrease in grain shape preferred orientation of all felsic phases. To explain these data, a new petrogenetic model is proposed for the origin of felsic migmatites by melt infiltration from an external source into banded orthogneiss during deformation. In this model, infiltrating melt passes pervasively along grain boundaries through the whole-rock volume and changes completely its macro- and microscopic appearance. It is suggested that the individual migmatite types represent different degrees of equilibration between the host rock and migrating melt during exhumation. The melt topology mimicked by feldspar in banded orthogneiss forms elongate pockets oriented at a high angle to the compositional banding, indicating that the melt distribution was controlled by the deformation of the solid framework. The microstructure exhibits features compatible with a combination of dislocation creep and grain boundary sliding deformation mechanisms. The migmatite microstructures developed by granular flow accompanied by melt-enhanced diffusion and/or melt flow. However, an AMS study and quartz microfabrics suggest that the amount of melt present did not exceed a critical threshold during the deformation to allow free movements of grains. [source] The role of the pathologist in translational and personalized medicineMOUNT SINAI JOURNAL OF MEDICINE: A JOURNAL OF PERSONALIZED AND TRANSLATIONAL MEDICINE, Issue 1 2007Daniel P. Perl MD Abstract Over the years, pathologists have served to make morphologic diagnoses for clinicians when provided with a biopsy or surgically resected tissue specimen. Traditionally, pathologists have used a series of morphologic techniques and relied on the microscopic appearance of resected tissues to determine a pathologic diagnosis and, with respect to neoplastic lesions, provide predictions of the potential growth pattern that might be anticipated. With the introduction of the techniques of molecular biology in medicine, the role of the pathologist has changed as have the tools available for characterizing pathologic specimens. With the pathologist's unique perspective on disease processes and access to tissue specimens from the operating room, he has become a key player in the area of translational and personalized medicine and the development of new approaches to diagnosis and translational research. Mt Sinai J Med 74:22,26, 2007. © 2007 Mount Sinai School of Medicine [source] Disruption of axoplasmic transport induces mechanical sensitivity in intact rat C-fibre nociceptor axonsTHE JOURNAL OF PHYSIOLOGY, Issue 2 2008Andrew Dilley Peripheral nerve inflammation can cause axons conducting through the inflamed site to become mechanically sensitive. Axonal mechanical sensitivity (AMS) of intact axons may explain symptoms in a diverse number of conditions characterized by radiating pain evoked by movements of the affected nerve. Because nerve inflammation also disrupts axoplasmic transport, we hypothesized that the disruption of axoplasmic transport by nerve inflammation could cause the cellular components responsible for mechanical transduction to accumulate and become inserted at the inflamed site, causing AMS. This was tested by examining AMS in C-fibre nociceptors following the application of axoplasmic transport blockers (colchicine and vinblastine) to the sciatic nerve. Both 10 mm colchicine and 0.1 mm vinblastine caused AMS to develop in 30.6% and 33.3% of intact axons, respectively (P < 0.05 compared to sham treatment). Since high doses of colchicine (> 50 mm) can damage axons, and inflammation is involved in the removal of axonal debris, experiments were performed to assess conduction across the treatment site as well as signs of inflammation. Results indicated minimal axonal loss (95% of A- and C-fibres conducting), consistent with the normal microscopic appearance of the colchicine treatment site and absence of ED1-positive (recruited) macrophages. In a separate series of experiments, the block of axoplasmic transport proximal to a localized neuritis significantly reduced inflammation-induced AMS (15.6% compared to 55.6%; P < 0.05), further supporting that the components necessary for AMS are moved by anterograde transport. In summary, nerve inflammation that causes the disruption of axoplasmic transport in patients with painful conditions may result in the accumulation and insertion of mechanosensitive elements at the inflamed site. [source] Pathological and clinical significance of increased intraepithelial lymphocytes (IELs) in small bowel mucosa,APMIS, Issue 6 2005Review article Intestinal intraepithelial lymphocytes (IELs) belong to a unique T-cell population interspersed between epithelial cells of both the small and large intestine. It is becoming increasingly recognised that an increased number of IELs with a normal villous architecture is within the wide spectrum of histological abnormalities observed in coeliac disease. An increased number of IELs is the earliest pathological change following gluten challenge and a high IEL count may be the only sign of gluten sensitivity. Therefore, the finding of a raised IEL count with normal villous architecture is of sufficient clinical importance to be reported in routine small bowel biopsies. However, it is evident that not all small intestinal biopsy specimens showing increased IELs are explained by gluten sensitivity. Increased IELs in small bowel mucosa have also been associated with autoimmune disorders, tropical sprue, food protein intolerance, Helicobacter pylori -associated gastritis, peptic duodenitis, parasitic and viral infections, as well as the development of intestinal lymphoma. Histological examination of a biopsy specimen of the small bowel remains the diagnostic gold standard for coeliac disease. There will be an ever increasing demand for histological confirmation of gluten sensitivity in patients in whom the classic microscopic appearance of flattened villi may not have fully developed. The more widespread recognition by histopathologists of the pattern of injury manifested by increased numbers of IELs in intestinal biopsy specimens will certainly help in early diagnosis of coeliac disease, lessen diagnostic confusion and influence the modern practice of gastrointestinal tract medicine. This review discusses some of the recent developments in clinical pathology pertaining to increased IELs in small bowel mucosal biopsies. [source] Uncoupling of intestinal mitochondrial oxidative phosphorylation and inhibition of cyclooxygenase are required for the development of NSAID-enteropathy in the ratALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 5 2000Somasundaram Background: The pathogenesis of NSAID-induced gastrointestinal damage is believed to involve a nonprostaglandin dependent effect as well as prostaglandin dependent effects. One suggestion is that the nonprostaglandin mechanism involves uncoupling of mitochondrial oxidative phosphorylation. Aims: To assess the role of uncoupling of mitochondrial oxidative phosphorylation in the pathogenesis of small intestinal damage in the rat. Methods: We compared key pathophysiologic events in the small bowel following (i) dinitrophenol, an uncoupling agent (ii) parenteral aspirin, to inhibit cyclooxygenase without causing a ,topical' effect and (iii) the two together, using (iv) indomethacin as a positive control. Results: Dinitrophenol altered intestinal mitochondrial morphology, increased intestinal permeability and caused inflammation without affecting gastric permeability or intestinal prostanoid levels. Parenteral aspirin decreased mucosal prostanoids without affecting intestinal mitochondria in vivo, gastric or intestinal permeability. Aspirin caused no inflammation or ulcers. When dinitrophenol and aspirin were given together the changes in intestinal mitochondrial morphology, permeability, inflammation and prostanoid levels and the macro- and microscopic appearances of intestinal ulcers were similar to indomethacin. Conclusions: These studies allow dissociation of the contribution and consequences of uncoupling of mitochondrial oxidative phosphorylation and cyclooxygenase inhibition in the pathophysiology of NSAID enteropathy. While uncoupling of enterocyte mitochondrial oxidative phosphorylation leads to increased intestinal permeability and low grade inflammation, concurrent decreases in mucosal prostanoids appear to be important in the development of ulcers. [source] | ||||||||||