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131.
Immunohistochemical evaluation of T cells in oral lesions from human immunodeficiency virus-positive persons with oropharyngeal candidiasis
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Myers TA Leigh JE Arribas AR Hager S Clark R Lilly E Fidel PL 《Infection and immunity》2003,71(2):956-963
Oropharyngeal candidiasis (OPC), caused by Candida albicans, is the most frequent opportunistic fungal infection in human immunodeficiency virus (HIV)-positive persons. Although Th1-type CD4(+) T cells are considered important for host defense against mucosal C. albicans infections, there is a paucity of information regarding the presence and/or role of T cells in OPC lesions. In pursuit of this, initial chromophore immunohistochemical studies showed a majority of CD8(+) rather than CD4(+) cells equally distributed throughout the buccal mucosa of OPC(-) persons (HIV(-) or HIV(+)), irrespective of blood CD4(+) cell numbers. In contrast, CD8(+) cells in lesions from HIV(+) OPC(+) persons were in significantly higher numbers and concentrated at the lamina propria-epithelium interface, a considerable distance from the Candida at the outer epithelium. Dual fluorescence and confocal microscopy confirmed that the majority of CD8(+), but not CD4(+), cells were T cells by the presence or absence, respectively, of CD3 on each cell type. These results suggest that CD8(+) T cells may be important for oral host defense against OPC, especially when CD4 cell numbers are reduced, with a potential CD8 cell-specific dysfunction associated with susceptibility to OPC. 相似文献
132.
P A Hofer R Anderson 《Acta pathologica et microbiologica Scandinavica. Section A, Pathology》1975,83(3):309-322
The pathology of primary familia amyloidosis with polyneuropathy is described on the basis of post-mortem examination of six cases from Northern Sweden. Clinically the disease is characterized by progressive sensory and motor disturbances with loss of sensation, muscular wasting and flaccid paralysis. Impotence, urinary bladder dysfunction, motility disturbances of the gastro-intestinal tract and postural hypotension indicate affection of the autonomic nervous system as well. Malabsorption, cardiac insufficiency and vitreous opacites also occur. As regards the distribution of amyloid, the following findings seemed to be characteristic. Usually there were no gross lesions indicating the amyloid disease. Histopathologically, amyloid deposits were observed in great extent in the peripheral nervous system and in various parts of the peripheral autonomic nervous system as well. It occurred extensively in the walls of blood vessels of various calibres, in the perivascular collagenous connective tissue and adjacent to the smooth musculature. Amyloid deposition was also found more or less abundantly in various other organs and tissues. No deposits, however, or only insignificant amounts, were found in the central nervous system, either in the parenchyma of the liver, in the islets of Langerhans, or in the bone marrow. Clinical manifestations seemed to be related to the local deposition of the amyloid substance. Our clinical and pathological findings in this particular type of familial amyloidosis conformed mostly to those previously described. 相似文献
133.
M A Hofer 《Psychosomatic medicine》1970,32(6):633-647
134.
Constitutive retinal CD200 expression regulates resident microglia and activation state of inflammatory cells during experimental autoimmune uveoretinitis 总被引:6,自引:0,他引:6
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Broderick C Hoek RM Forrester JV Liversidge J Sedgwick JD Dick AD 《The American journal of pathology》2002,161(5):1669-1677
Recent evidence supports the notion that tissue OX2 (CD200) constitutively provides down-regulatory signals to myeloid-lineage cells via CD200-receptor (CD200R). Thus, mice lacking CD200 (CD200(-/-)) show increased susceptibility to and accelerated onset of tissue-specific autoimmunity. In the retina there is extensive expression of CD200 on neurons and retinal vascular endothelium. We show here that retinal microglia in CD200(-/-) mice display normal morphology, but unlike microglia from wild-type CD200(+/+) mice are present in increased numbers and most significantly, express inducible nitric oxide synthase (NOS2), a macrophage activation marker. Onset and severity of uveitogenic peptide (1-20) of interphotoreceptor retinoid-binding protein-induced experimental autoimmune uveoretinitis is accelerated in CD200(-/-) mice and although tissue destruction appears no greater than seen in CD200(+/+) mice, there is continued increased ganglion and photoreceptor cell apoptosis. Myeloid cell infiltrate was increased in CD200(-/-) mice during experimental autoimmune uveoretinitis, although NOS2 expression was not heightened. The results indicate that the CD200:CD200R axis regulates retinal microglial activation. In CD200(-/-) mice the release of suppression of tonic macrophage activation, supported by increased NOS2 expression in the CD200(-/-) steady state accelerates disease onset but without any demonstration of increased target organ/tissue destruction. 相似文献
135.
Effect of exercise on coronary endothelial function in patients with coronary artery disease 总被引:36,自引:0,他引:36
Hambrecht R Wolf A Gielen S Linke A Hofer J Erbs S Schoene N Schuler G 《The New England journal of medicine》2000,342(7):454-460
BACKGROUND: Studies of the cardioprotective effects of exercise training in patients with coronary artery disease have yielded contradictory results. Exercise training has been associated with improvement in myocardial perfusion even in patients who have progression of coronary atherosclerosis. We therefore conducted a prospective study of the effect of exercise training on endothelial function in patients with coronary artery disease. METHODS: We randomly assigned 19 patients with coronary endothelial dysfunction, indicated by abnormal acetylcholine-induced vasoconstriction, to an exercise-training group (10 patients) or a control group (9 patients). To reduce confounding, patients with coronary risk factors that could be influenced by exercise training (such as diabetes, hypertension, hypercholesterolemia, and smoking) were excluded. In an initial study and after four weeks, the changes in vascular diameter in response to the intracoronary infusion of increasing doses of acetylcholine (0.072, 0.72, and 7.2 microg per minute) were assessed. The mean peak flow velocity was measured by Doppler velocimetry, and the diameter of epicardial coronary vessels was measured by quantitative coronary angiography. RESULTS: In the initial study, the two groups had similar vasoconstrictive responses to acetylcholine. After four weeks of exercise training, coronary-artery constriction in response to acetylcholine at a dose of 7.2 microg per minute was reduced by 54 percent (from a mean [+/-SE] decrease in the luminal diameter of 0.41+/-0.05 mm in the initial study to a decrease of 0.19+/-0.07 mm at four weeks; P<0.05 for the comparison with the change in the control group). In the exercise-training group, the increases in mean peak flow velocity in response to 0.072, 0.72, and 7.2 microg of acetylcholine per minute were 12+/-7, 36+/-11, and 78+/-16 percent, respectively, in the initial study. After four weeks of exercise, the increases in response to acetylcholine were 27+/-7, 73+/-19, and 142+/-28 percent (P<0.01 for the comparison with the control group). Coronary blood-flow reserve (the ratio of the mean peak flow velocity after adenosine infusion to the resting velocity) increased by 29 percent after four weeks of exercise (from 2.8+/-0.2 in the initial study to 3.6+/-0.2 after four weeks; P<0.01 for the comparison with the control group). CONCLUSIONS: Exercise training improves endothelium-dependent vasodilatation both in epicardial coronary vessels and in resistance vessels in patients with coronary artery disease. 相似文献
136.
We present 3 adults with cardiac rhabdomyomas, 2 in the atria and 1 in the right ventricle. One atrial tumor was discovered incidentally, and 1 resulted in supraventricular tachycardia. The ventricular lesion caused ventricular tachycardia. Compared with congenital rhabdomyomas, the tumors are relatively cellular, the cells are smaller, there are few spider cells, and there is evidence of cell proliferation. Two of the 3 tumors demonstrated spindling in contrast to adult rhabdomyomas of the head and neck. Although surgical excision was possible in all patients, long-term follow-up will be required to determine the true biologic behavior of these neoplasms. 相似文献
137.
Meg Stuart Jane E. Butler David F. Collins Janet L. Taylor Simon C. Gandevia 《The Journal of physiology》2002,545(3):731-737
Many freshwater turtles in temperate climates may experience winter periods trapped under ice unable to breathe, in anoxic mud, or in water depleted of O2 . To survive, these animals must not only retain function while anoxic, but they must do so for extended periods of time. Two general physiological adaptive responses appear to underlie this capacity for long-term survival. The first is a coordinated depression of metabolic processes within the cells, both the glycolytic pathway that produces ATP and the cellular processes, such as ion pumping, that consume ATP. As a result, both the rate of substrate depletion and the rate of lactic acid production are slowed greatly. The second is an exploitation of the extensive buffering capacity of the turtle's shell and skeleton to neutralize the large amount of lactic acid that eventually accumulates. Two separate shell mechanisms are involved: release of carbonate buffers from the shell and uptake of lactic acid into the shell where it is buffered and sequestered. Together, the metabolic and buffering mechanisms permit animals to survive for 3–4 months at 3 °C with no O2 and with circulating lactate levels of 150 mmol l−1 or more. 相似文献
138.
139.
Winifred W. Barouch Kimberly E. Breese Stephanie -Alexis Davidoff John Leszyk Andrew G. Szent-Györgyi Janet L. Theibert John H. Collins 《Journal of muscle research and cell motility》1991,12(4):321-332
Summary We have determined the amino acid sequences of the essential light chains (ELC) and regulatory light chains (RLC) of myosin from two species of clam,Mercenaria mercenaria andMacrocallista nimbosa, using protein chemistry methods. The N-termini of all four proteins were blocked, and sequencing was carried out on various chemically and enzymatically produced peptide fragments. Cleavage of eitherMercenaria RLC (MRLC) orMacrocallista RLC (VLC) at its 3 Arg yielded four peptides, three of which could not be sequenced directly, due to an N-terminal blocking group and 2 Arg-Gln bonds in these proteins. The fourth peptide was partially and specifically cleaved at an unusually reactive residue, Met-64, which is invariant in all known RLC sequences. A comparison of all available molluscan ELC and RLC sequences was carried out in search of clues to functionally important features of these proteins in muscles which are regulated by a Ca2+-sensitive myosin. By analogy with other RLCs, VRLC and MRLC may be phosphorylated at Ser-11 by an endogenous kinase. All myosin light chains, like troponin C and calmodulin, contain four homologous regions, I to IV, each of which contains a twelve-residue potential Ca2+-binding loop flanked on either side by a pair of helices. All RLCs, including those from Ca2+-insensitive myosins, contain a divalent cation-binding site in region I. Clam and other molluscan ELCs contain a single Ca2+-binding site in region III. This site is present only in the ELCs of myosins that are regulated by direct binding of Ca2+. The ELC site III is likely to play a key role in the regulation of molluscan muscle contraction. 相似文献
140.
Cideciyan AV Aleman TS Swider M Schwartz SB Steinberg JD Brucker AJ Maguire AM Bennett J Stone EM Jacobson SG 《Human molecular genetics》2004,13(5):525-534
Mutations in ABCA4, which encodes a photoreceptor specific ATP-binding cassette transporter (ABCR), cause autosomal recessive forms of human blindness due to retinal degeneration (RD) including Stargardt disease. The exact disease sequence leading to photoreceptor and vision loss in ABCA4-RD is not known. Extrapolation from murine and in vitro studies predicts that two of the earliest pathophysiological features resulting from disturbed ABCR function in man would be slowed kinetics of the retinoid cycle and accelerated deposition of lipofuscin in the retinal pigment epithelium (RPE). To determine the human pathogenetic sequence, we studied surrogate measures of retinoid cycle kinetics, lipofuscin accumulation, and rod and cone photoreceptor and RPE loss in ABCA4-RD patients with a wide spectrum of disease severities. There were different extents of photoreceptor/RPE loss and lipofuscin accumulation in different regions of the retina. Slowing of retinoid cycle kinetics was not present in all patients; when present, it was not homogeneous across the retina; and the extent of slowing correlated well with the degree of degeneration. The orderly relationship between these phenotypic features permitted the development of a model of disease sequence in ABCA4-RD. The model predicted lipofuscin accumulation as a key and early component of the disease expression in man, as in mice. In man, however, abnormal slowing of the rod and cone retinoid cycle occurs at later stages of the disease sequence. Knowledge of the human ABCA4 disease sequence will be critical for defining rates of progression, selecting appropriate patients and retinal locations for future therapy, and choosing appropriate treatment outcomes. 相似文献