Knee pain: a clue to internal derangement on lateral plain radiograph of the knee.
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Adult↗
Biomedical subjects
C Romano
Publications and source records attributed to C Romano.
Case report of a monoclonal gammopathy in a patient with chronic hepatitis: effects of beta-IFN treatment.
A sixty-one-year-old woman, with cirrhosis, presented with a monoclonal gammopathy of uncertain significance (MGSU). Often in a condition of cirrhosis is present a benign M component hypergammaglobulinemia. The electrophoresis and the immunophoresis showed a dense papraprotein in the gamma-region, an IgG with K light chain, an uncertain Bence-Jones proteinuria, a medullary plasmacytosis (9%), and a following growth of paraprotein were present. Lymphoblastic plasma cell were absent. Treatment with beta-IFN 6 MU for a period of six months and 3 MU for a further period of three months proved ineffective for hepatic disease, but produced a quantitative reduction in gamma-G globulin, the Bence-Jones proteinuria was absent, a reduction in M component and in medullary plasmacytosis. Electrophoresis showed a polyclonal evolution of the gammopathy. Suspension of treatment was followed by de novo rise of monoclonal immunoglobulin. The authors report the use of beta-IFN in the therapy of multiple myeloma.
Antiviral Agents↗
[Radiographic manifestations in teeth and jaws in chronic kidney insufficiency].
Forty-five patients affected with chronic renal failure (29 men and 16 women; mean age: 47.8 years), treated with hemodialysis for 4 to 245 months (mean: 66.9 months) were examined with panoramic and skeletal radiographs-the latter of the skull, hands, shoulders and clavicles, pelvis and spine. The control group (45 subjects with no renal diseases) was examined only with panoramic radiography. Dental and skeletal radio-graphs were given an 0-6 score and then compared to assess a possible relationship between skeletal and dental changes at radiography. Twenty-six dialysis patients (57.7%) had radiographic abnormalities in the maxillary bones-i.e., osteoporosis (100% of patients), focal osteosclerosis adjacent to the roots (11.5%), lamina dura reduction or loss (26.9%), calcifications of soft tissues or salivary glands (15.3%) and brown tumors (7.6%). In the teeth of dialysis patients, the dental pulp chamber was narrowed in 11.1% and hypercementosis of the roots was observed in 4.5%. Radiographic abnormalities in the hand, shoulder and pelvis were depicted in 51.1% of dialysis patients-in 86.9% of them with maxillary lesions. In the control group, 15.5% had mandibular bone lesions-i.e., osteopenia, cortex reduction at the mandibular angles and cyst-like lesions -but the evidence of caries and periodontal disease did not differ from that in the dialysis group. The diagnosis and follow-up of dialysis patients are currently made with serum biochemistry, radiography and histology. The purpose of skeletal radiology is to monitor the progression or regression of musculoskeletal abnormalities. Panoramic radiography might be useful in monitoring renal osteodystrophy, especially to assess the response to therapy-i.e., parathyroidectomy, calcium or vitamin-D therapy and renal transplant.
Adult↗
[Hepatitis C].
HCV carriers are supposed to me 100,000,000 worldwide. 5-15% of subjects are infected via haemotransfusion and another significant amount via intravenous drugs; nevertheless in the major part of subjects the via of transmission remains unclear. HCV causes long-term infectious in the host because of its high frequency of mutations. Mutations origin multiple mutants, called quasi-species, who have distinct immunological features and can so easily escape host immune response. Chronic HCV infection leads to cirrhosis in 5-10 years and to a possible hepatocarcinoma in 15-20 years. Nevertheless, it remains unclear why some patients undergo a slight clinical course, while others experience an aggressive one (exitus in less than 5 years). Alpha-interferon (alpha-IFN) is at date the only drug of proven efficacy in HCV chronic hepatitis, even if HCV eradication is a rare event. The goal to obtain is to standardize doses and duration of the treatment.
Adult↗
Metabotropic glutamate receptor mGluR5 subcellular distribution and developmental expression in hypothalamus.
The metabotropic glutamate receptor mGluR5 is a G-protein coupled receptor that plays a key role in release of Ca2+ from internal stores via inositol triphosphate mobilization. Western and Northern blot analyses revealed a greatly enhanced expression of mGluR5 in rats during early stages of hypothalamic development compared with the adult. This enhanced developmental expression provides an explanation for the dramatic physiological response of developing neurons to metabotropic glutamate receptor activation and supports the argument that metabotropic glutamate receptors may play an important role in hypothalamic development. During development, expression of the mGluR5 gene was reduced, not only in the hypothalamus but also in other regions of the brain. A differential decrease in mGluR5 protein was found in different brain regions with Western blot analysis. The hypothalamus showed a sixfold decrease in mGluR5 with development, whereas the cortex showed only a threefold decrease. Immunocytochemistry with an affinity-purified antibody against a peptide deduced from the cloned mGluR5 gene revealed selective expression in some regions in the adult hypothalamus. In the adult and developing (postnatal day 10) brain, immunoreactive neurons were found in the suprachiasmatic nucleus, preoptic area, lateral hypothalamus, and mammillary region, areas where the related metabotropic glutamate receptor mGluR1 is also found. In contrast, the ventromedial nucleus, an area critically involved in the regulation of food intake and metabolic balances, showed strong mGluR5 immunoreactivity but no mGluR1 immunoreactivity. Little or no mGluR5 staining was found in the neurosecretory neurons of the paraventricular, supraoptic, and arcuate nuclei. Ultrastructurally, mGluR5 was associated with the cytoplasmic face of the plasmalemma on hypothalamic dendrites, dendritic spines, and neuronal perikarya in the adult. The strongest immunoreactivity was found in patches on the membrane, sometimes associated with the postsynaptic side of synapses and sometimes associated with nonsynaptic dendritic or perikaryal membrane. Intense immunostaining was found on some astrocyte processes surrounding synaptic complexes containing asymmetrical synapses. These astrocytes would be in an ideal position to receive excitatory signals from glutamatergic axons. Unlike the punctate appearance of immunolabeling on neuronal membranes, astrocytes showed continuous staining along the plasma membrane.
Animals↗
Roles of metabotropic glutamate receptors in brain plasticity and pathology.
In summary, the mGluRs are a large family of receptor subtypes with diverse properties in terms of transduction coupling, pharmacology, and anatomical distribution. Many divergent studies have demonstrated that activation of these receptors can result in either neuroprotection or neuropathology. We hypothesized that the mGluRs of astrocytes may have a role in determining the response following administration of mGluR agonists in vivo, and we have defined a suitable in vitro model for the study of these receptors. The experimental plasticity demonstrated in the astrocyte culture model may represent a more general principle that conditions in the microenvironment may differentially alter mGluR subtype expression as part of development, functional specialization, or pathology. This astrocyte model of receptor regulation provides a system suitable for studying the effects of specific growth factors, neurotrophins, cytokines, and other substances released by neurons and glia that may act in both autocrine and paracrine fashions. Alteration in the ratios of receptors by such variables could then modify future signaling properties and neuroglial interactions, a form of conditioning of the astrocytic response that would alter the physiological output following glutamate release. One measure of the value of this model will be its usefulness in stimulating the generation of hypotheses that can be tested in vivo. For example, the morphology of the astrocytes when cultured in the defined medium has similarities to the morphology of astrocytes undergoing reactive gliosis in pathological states. It is also interesting to note that treatments that have been reported to increase excitatory amino acid-stimulated PI hydrolysis in ex vivo brain slices (lesions, ischemia, and kindling) are accompanied by reactive gliosis. Those findings combined with the present in vitro results lead us to speculate that mGluR5 expression may also be altered in vivo during reactive gliosis. If so, it will be important to examine the functional consequences of such a change with regard to the astrocytic response to injury and maintaining the balance between excitatory transmission and excitotoxicity.
Animals↗
Distribution of metabotropic glutamate receptor mGluR5 immunoreactivity in rat brain.
The receptor mGluR5 is a metabotropic glutamate receptor with messenger RNA abundantly present throughout cortex, hippocampus, and caudate/putamen that is also coupled to phosphatidyl inositide hydrolysis and calcium mobilization. In this study, the distribution of mGluR5 was examined in rat brain by immunocytochemistry. The antibody utilized is highly specific and does not cross react with the most closely related other metabotropic glutamate receptor, as determined by Western blot analysis of nonneuronal cells transfected with metabotropic receptor coding sequences. The receptor mGluR5 is widely expressed with the highest density in olfactory bulb, caudate/putamen, lateral septum, cortex, and hippocampus, as confirmed with both immunocytochemistry and Western blot analysis. Electron microscopic studies in hippocampus and cortex indicate that the labeling is mostly on membranes of dendritic spines and shafts. Light and electron microscopic evidence indicates that some mGluR5 immunoreactivity is located in presynaptic axon terminals, suggesting that mGluR5 may function as a presynaptic receptor.
Amino Acid Sequence↗
Immunohistochemical study of two phosphoinositide-linked metabotropic glutamate receptors (mGluR1 alpha and mGluR5) in the cat visual cortex before, during, and after the peak of the critical period for eye-specific connections.
The distribution of two phosphoinositide-linked metabotropic glutamate receptors (mGluR1 alpha and mGluR5) was studied immunohistochemically in area 17 before, during and after the peak of use-dependent modification of eye-specific connections. In the adult, mGluR1 alpha immunoreactivity is high in all layers except layer IV, where mGluR5 immunoreactivity is concentrated. This difference in distribution indicates different functions for these two receptor subtypes. The laminar pattern of mGluR1 alpha immunoreactivity is similar in all three ages, but the overall labeling intensity decreases after the peak (6 weeks of age) of the critical period. The laminar pattern of mGluR5 immunoreactivity changes with age. It is expressed in most layers at 2 days of age and is found mainly in layer IV in the adult. This laminar distribution and developmental pattern match the distribution and the development of the geniculocortical terminals. The change in mGluR1 alpha labeling intensity and mGluR5 laminar distribution over time is consistent with both of these mGluRs being involved in sensory-dependent plasticity for eye-specific connections in the visual cortex.
Animals↗
Electrophysiological evidence of "nerve entrapment syndromes" and subclinical peripheral neuropathy in progressive systemic sclerosis (scleroderma).
We report the electrophysiological findings and the management of 5 subjects with progressive systemic sclerosis (PSS) and clinical evidence of nerve entrapment. Three had carpal tunnel syndrome (CTS), 1 bilateral CTS and right tarsal tunnel syndrome (TTS) and 1 Guyon's canal syndrome. Only 1 patient (with CTS) showed significant clinical improvement after surgical decompression; the other 4 demonstrated a slight recovery of conduction without lasting clinical relief after conventional treatment. To explain these failures we hypothesized that these entrapment syndromes were the clinical expression of underlying diffuse damage to the peripheral nervous system (PNS). The conduction values of nerves unaffected by entrapment syndromes were within normal limits, but almost all distal velocities were below the mean of controls. Such subclinical distal peripheral neuropathy was also verified in a selected sample of 17 patients with PSS, without clinical symptoms or signs of PNS involvement. In these 17 cases the mean distal sensory and motor conduction findings of the median, ulnar, sural and tibial nerves were significantly lower than those of a control group, while no significant differences were found in the more proximal tracts of the same nerves. Furthermore, 3 of the 17 patients showed classical electrophysiological evidence of TCS and TTS without any clinical symptoms. We conclude that the subjects with PSS had subclinical polyneuropathy which may become plain polyneuropathy or nerve entrapment syndromes perhaps induced by other risk factors.
Adult↗
Blockade of the second messenger functions of the glutamate metabotropic receptor is associated with degenerative changes in the retina and brain of immature rodents.
Activation of metabotropic glutamate receptors (mGluR) by Glu or related mGluR agonists triggers phosphoinositide (PI) hydrolysis, intracellular Ca2+ mobilization and protein kinase C activation. These mGluR agonist-stimulated events are inhibited strongly by 2-amino-3-phosphono-L-propionic acid (L-AP3) and L-aspartate-beta-hydroxamate (L-A beta H), and much more weakly by D-AP3 and L-serine-O-phosphate (L-SOP). Daily s.c. administration of DL-AP3 subchronically to infant rodents causes the developing retina and optic nerves to degenerate. In the present study, we describe the evolution of the cytopathological reaction in the developing rodent retina following DL-AP3 treatment and show that DL-AP3 can induce similar cytopathological changes in several regions of the immature rodent brain. In addition, we show that the retinotoxic action of DL-AP3 is mimicked by L-A beta H but not by L-SOP, and that L-AP3 is a much stronger retinotoxin that D-AP3. These observations suggest a possible mechanistic link between the PI-hydrolysis blocking action and retinotoxic action. Our findings are consistent with the hypothesis that under normal physiological circumstances, the Glu metabotropic receptor through its PI-hydrolysis-linked second messenger functions provides vitally important support for developing neurons, and that disruption of this support can cause widespread neuronal degeneration.
Alanine↗
Delayed excitotoxic neurodegeneration induced by excitatory amino acid agonists in isolated retina.
Evidence from in vitro studies suggests that excitotoxic neuronal degeneration can occur by either an acute or delayed mechanism. Studies of the acute mechanism in isolated chick embryo retina using histological methods indicate that this process is rapidly triggered by activation of glutamate receptors of either the N-methyl-D-aspartate (NMDA) or non-NMDA subtypes. The delayed mechanism, studied primarily in cortical and hippocampal cell cultures prepared from embryonic rodent brain, requires activation of NMDA receptors. In these cell culture systems, stimulation of non-NMDA receptors does not rapidly trigger delayed neuronal degeneration, or does so only indirectly, via activation of NMDA receptors secondary to glutamate release. To provide a more valid basis for comparison of these two mechanisms, we have modified the isolated chick embryo retina model to permit studies of delayed as well as acute excitotoxic neurodegeneration. Retinas maintained for 24 h exhibited no morphological or biochemical signs of damage. Retinal damage was assessed by measuring lactate dehydrogenase (LDH) present in the medium at various times after exposure to agonists and normalized to total LDH in each retina. Glutamate exposure (1 mM, 30 min) did not result in LDH release by the end of the exposure period, but LDH was released over the following 24 h. Briefer periods also led to substantial LDH release. Incubation in the presence of NMDA, or the non-NMDA agonists kainate (KA) or alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), led rapidly to delayed LDH release.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Factors related to the development of sensitization to green coffee and castor bean allergens among coffee workers.
BACKGROUND: Occupational allergic respiratory symptoms in coffee workers have been frequently reported, but the ultimate cause of sensitization is still debated, castor bean being considered besides green coffee beans. Atopy and cigarette smoking have been suggested as promoting factors of sensitization for several occupational allergens. OBJECTIVE: This study was carried out to assess the prevalence of allergic respiratory symptoms and of sensitization to both green coffee beans and castor bean in the whole workforce of a coffee manufacturing plant. Furthermore we wanted to ascertain both the presence of castor bean antigens in the settled dust of the green coffee beans warehouse and the possible crossreactivity between the two beans. Meanwhile, the effect of smoking and atopy was considered. METHOD: Two-hundred and eleven workers were examined. A questionnaire on oculorhinitis and asthma was administered and skin-prick tests for green coffee beans, castor bean and 15 common inhalant allergens were carried out. Isoelectric focusing, isoelectric focusing immunoblot and radioallergosorbent assay (RAST) inhibition were performed on samples of settled environmental dust from the green coffee area, as well as on castor bean and green coffee beans. RESULTS: Ten per cent of the workers complained of oculorhinitis alone and 16% of asthma (nearly always associated with oculorhinitis). The overall prevalence of skin-sensitization was: 15% for green coffee beans, 22% for castor bean, 22% for common allergens. Evidence of sensitization to occupational allergens was more common in smokers, with a more than twofold increase in relative risk. The strong association between skin positivity to common and occupational allergens suggests that atopy acts as an enhancing host factor towards occupational sensitization. The analysis of the dust confirmed the presence of castor bean antigens. CONCLUSION: Our findings indicate that castor bean is the major cause of occupational sensitization among coffee workers, whereas smoking and atopy act as enhancing factors.
Adult↗
A case of FG syndrome with gingival hyperplasia and keloids.
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Abnormalities, Multiple↗
Final height of girls with Turner's syndrome: correlation with karyotype and parental height.
Final height of 75 adults with Turner's syndrome (45 Israeli, 30 Italian), never treated with GH, was examined to see if a relationship with karyotype patterns and parental height existed. Patients were divided into five groups according to their chromosome pattern, as follows: group A = 45, X karyotype (34 patients); group B = mosaicism (11 with karyotype 45,X/46,XX and 7 with karyotype 45,X/46,XY); group C = deletion of all or part of Xp (19 patients); subgroup C1 = 6 with complete deletion of Xp; subgroup C2 = 9 with mosaicism 45,X/46,X,i(Xq); subgroup C3 = 4 with 45,X/46,X,ring(X); group D = deletion of Xq (4 patients); pure gonadal dysgenesis (PGD) group = 9 patients with pure 46,XX gonadal dysgenesis. No statistical difference was noted between the mean height of the two national populations studied (Italian 142.2 +/- 5.7 and Israeli 143.0 +/- 7.2 cm). The mean heights of group D (148.9 cm; range 147-166.2) and the PGD group (156.0 cm; 141-171.5) were found to be significantly higher than those observed in groups A, B and C (p < 0.03, p < 0.02 and p < 0.02, respectively), even though gonadal distinction existed in all five groups. Subgroup C1, where a deletion of the entire Xp segment [46,X,i(Xq)] was present, was found to be the shortest group (median height 134.5; range 131.9-138 cm).(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Behavior of soluble intercellular adhesion molecule-1 and endothelial-leukocyte adhesion molecule-1 concentrations in patients with Graves' disease with or without ophthalmopathy and in patients with toxic adenoma.
Expression of intercellular adhesion molecule-1 (ICAM-1) and endothelial-leukocyte adhesion molecule-1 (ELAM-1) on endothelium can be considered a critical early step for leukocyte migration from blood to tissues during inflammatory processes. Increased circulating soluble ICAM-1 (sICAM-1) levels have been found in sera from patients with Graves' disease (GD) with or without ophthalmopathy. Serum soluble ELAM-1 (sELAM-1) levels have not been measured in these patients. The aim of this study was to clarify the behavior of sICAM-1 and sELAM-1 levels in patients with hyperthyroidism due to GD with or with or without ophthalmopathy and in hyperthyroid patients with toxic thyroid adenoma. We studied sICAM-1 and sELAM-1 levels in 130 subjects (age 23-54 yr), grouped as follows: group 1, 30 untreated hyperthyroid GD patients (21 females and 9 males) with active ophthalmopathy; group 2, 26 euthyroid GD patients (16 females and 10 males) with active ophthalmopathy; group 3, 33 hyperthyroid GD patients (22 females and 11 males) without ophthalmopathy; group 4, 11 untreated hyperthyroid patients (7 females and 4 males) with single toxic adenoma; and a control group of 30 healthy subjects (21 females and 9 males). sICAM-1 and sELAM-1 concentrations were measured by a sandwich enzyme linked immunosorbent assay (ELISA) method. Groups 1, 2, and 3 (P < 0.001 for all 3 groups) but not group 4 showed increased sICAM-1 levels compared with the control group. However, groups 1 and 2 (P < 0.001 for both) showed higher values of sICAM-1 than group 3, and group 1 showed higher sICAM-1 levels than group 2 (P < 0.002). Groups 1 and 2 (P < 0.001 for both) but not groups 3 and 4 showed sELAM-1 levels significantly higher than the control group and positively correlated to the severity score of Graves' ophthalmopathy (GO) (P < 0.002 for group 1 and < 0.01 for group 2). Our results confirm that increased sICAM levels in GD patients with or without ophthalmopathy (with higher levels in patients with GO) but not in hyperthyroid nonautoimmune patients may be the consequence of orbital and thyroid inflammation, and they also suggest that sICAM concentrations could reflect the degree of inflammatory activity. Increased sELAM-1 concentrations only, in patients with ophthalmopathy with or without hyperthyroidism significantly correlated to severity score of GO, suggest the measurement of sELAM-1 levels as a specific marker of endothelium activation in GO.
Adenoma↗
[Insulin edema in three adolescents with insulin-dependent diabetes mellitus].
Three female patients with a previously poorly controlled Insulin Dependent Diabetes Mellitus (IDDM), without evidence of cardiovascular, hepatic or renal dysfunction, developed generalized edema after a substantial increase in their insulin dosage. Edema resolved in 2-3 weeks, without specific therapy. Our patient's findings met the criteria of diagnosis of insulin edema. Insulin edema during IDDM is an uncommon complication of insulin therapy (1/400) and its pathogenesis is not clarified so far; it is a transient and self-limiting condition. The diagnosis is based on exclusion of all other major causes of edema.
Adolescent↗
Growth in patients after allogeneic bone marrow transplant for hematological diseases in childhood.
The growth of 66 long-term survivors, transplanted in two centres (Genoa S. Martino and Monza) is reported. Patients were all under age 15 at the time of bone marrow transplantation (mean 9.8 +/- 3.4 years; range 1.07-15 years) with a minimum follow-up of at least 12 months. They were divided into four groups. Group 1: eight patients with severe aplastic anemia (SAA): conditioning included cyclophosphamide (CY) 200 mg/kg only. Group 2: 32 patients with acute lymphoblastic leukemia (ALL), and acute myeloid leukemia (AML): conditioning included CY 120 mg/kg and 10-12 Gy fractionated total body irradiation (fTBI). Group 3: 20 patients with ALL, who had previously received cranial irradiation; conditioning included CY 120 mg/kg and fTBI with an additional testicular irradiation (4 Gy). Group 4: six patients with chronic myeloid leukemia (CML) and AML; conditioning included CY 200 mg/kg and busulfan (BU) 16 mg/kg. Group was impaired in all four groups, including the unirradiated groups (-0.2 +/- 0.7 and -0.5 +/- 0.6 delta-SDS in groups I and 4, respectively). Growth impairment-SDS was statistically significant in the two irradiated groups (-0.7 +/- 1.0 and -0.9 +/- 1.0 delta-SDS in groups 2 and 3, respectively), more marked in patients who had had previous cranial irradiation. Chronic graft-versus-host disease and its treatment were not found to have a major effect on growth.
Acute Disease↗
Anti-rhodopsin antibodies in sera from patients with normal-pressure glaucoma.
PURPOSE: To explore further the potential role autoimmunity may play in the pathogenesis of normal-pressure glaucoma (NPG) in some patients, the authors examined the sera of patients with NPG for the presence of antibodies directed toward retinal antigens. METHODS: Using patient sera, immunoblotting was performed on subcellular fractions of retina, purified bovine rhodopsin, and immunoaffinity-purified recombinant human rhodopsin. A chemiluminescence-enzyme-linked immunosorbent assay (ELISA) to detect anti-rhodopsin antibodies was developed and used. RESULTS: A patient with NPG was found to have a high titer of immunoglobulin M-lambda antibody against a 40-kd retina-specific glycoprotein antigen subsequently identified as rhodopsin. ELISA analysis conducted on sera from 28 patients with NPG and 26 patients with primary open-angle glaucoma (POAG) revealed highly significant differences in anti-rhodopsin antibody activity between these groups (P < 0.0002, Mann-Whitney test). For example, the majority of patients with NPG (19/28; 68%) had anti-rhodopsin antibody activity higher than the highest value obtained from among 26 age-matched patients with POAG. CONCLUSIONS: An elevated anti-rhodopsin antibody count is related to NPG. This may indicate that there is an autoimmune component in the optic neuropathy in these patients. The specific role of these autoantibodies, if any, in the pathogenesis of the disease remains to be determined.
Aged↗