Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A modified hemoglobin solution (<pyridoxylated hemoglobin>-<polyoxyethylene> conjugate solution, PHP solution) has very interesting characteristics such as oxygen-carrying property without corpuscular components. Experimental use of the PHP solution has shown promising possibilities as a perfusate relevant to organ transplantations. 1) Elongation of warm ischemic time in canine kidneys: Dogs survived even with the unilateral kidneys which had been exposed up to 4.5 hour warm ischemia and, thereafter, perfused with the PHP solution. 2) Elongation of perfusion preservation period of canine livers: Dogs survived with the transplanted livers which had been perfused for 48 hours with the PHP solution. 3) Successful perfusion of rat small intestine: Lewis rat intestines perfused and preserved for 12 hours with the PHP solution showed a higher survival rate compared with those with Collins or UW solution. 4) Removal of antibodies: By exchange transfusion with a total of 30-60 ml of the PHP solution, a Lewis rat hematocrit lowered to 5% while IgG went down to nil from 8970 mg/dl, IgA to 28 mg/dl from 118 mg/dl and IgM to 190 mg/dl from 897 mg/dl. This technique is expected to be applicable for removal of the naturally existing antibodies in xenotransplantation.
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PMID:Modified hemoglobin solution as possible perfusate relevant to organ transplantation. 139 75

Secretory component was assayed in serum and bile from 34 patients within 40 days after a first or a second (three cases) liver transplantation. Levels of serum secretory IgA and IgM and of a serum component referred to as immunoreactive free secretory component, identified by its reactivity with monoclonal and polyclonal antibodies specific to secretory component, were significantly elevated in all posttransplant patients compared with 45 healthy subjects and 10 kidney transplant patients (p less than 0.0001). The highest serum levels of bound secretory component and of immunoreactive free secretory component were observed in patients with acute rejection. The elevation of immunoreactive free secretory component was significantly higher in patients with rejection as compared with patients with a graft ischemia (p = 0.002) or an uncomplicated postoperative evolution (p = 0.01). The highest levels of immunoreactive free secretory component and secretory IgM were observed in a transplant patient with selective IgA deficiency. No significant difference was seen between the levels of serum immunoreactive free secretory component observed in patients with rejection and those of patients with cytomegalovirus hepatitis or sepsis. Immunoreactive free secretory component, secretory IgA and secretory IgM levels measured in the serum of three patients with primary nonfunction were lower than those observed in the other groups. Immunoreactive free secretory component bile/serum ratios calculated from 16 patients were significantly higher in patients with acute rejection than in infected patients. This study provides new insight into the mechanisms of increase of serum immunoreactive free secretory component, secretory IgA and secretory IgM in various types of liver dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serum and bile secretory immunoglobulins and secretory component during the early postoperative course after liver transplantation. 195 52

Seventy donor kidneys for transplant were studied with light microscopy (LM), electron microscopy (EM) and immunofluorescence (IM) for C3, C4, Clq, IgG, IgA, IgE, IgM, and antifibrin; the samples were taken just before transplanting the allograft kidney. Glomerular changes were found in 35.7% of apparently normal living donors: 9 cases showed relative glomerular ischemia with an irregular basal membrane (12.9%); 5 cases showed a diffusely widened basal membrane without antecedents of hyperglycemia (7.1%); in one case (1.4%) there was a lesion similar to type 1 mesangio-capillary glomerulonephritis with C3++, IgG++, IgA+, and IgM+; in another case (1.4%) there were scant isolated C3 glomerular, subepithelial deposits with indentation of the basement membrane of the immunocomplex type with a microhematuria which was demonstrated only after donation, and in 9 cases (among them two pairs of siblings) there were mesangial IgA and mesangial electron-dense deposits compatible with Berger's disease (12.9%). None of these glomerulopathies were evident under LM.
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PMID:Morphological findings in 70 kidneys of living donors for renal transplant. 214 95

Samples from 103 kidneys donated for transplant were studied under light microscopy (LM), electron microscopy (EM) and immunofluorescence (IM, with C3, C4, C1q, IgG, IgA, IGE, IgM and antifibrin) just before transplantation. Seven kidneys were obtained from a cadaver (CK). Glomerular damage attributed to perfusion (perfusion glomerulopathy) was present in 4 cases. Glomerular changes in apparently healthy donors were present in 33% of cases: minor glomerular lesions, such as type I collagen fibers in the mesangial matrix (3 cases); uniform widening of the basal membrane without prior evidence of diabetes (4); relative glomerular ischemia with basal membrane irregularities (9). Major lesions were found in 17.5% of kidneys: IgA mesangial deposits compatible with Berger's disease (9, including 2 pairs of siblings); dense mesangial deposits suggesting the same process (6); subacute bacterial endocarditis glomerulopathy with IgG++, C1q+ and IgM+ (1, a CK); a type I mesangio-capillary glomerulonephritis with C3++, IgG++, IgA+ and IgM+ (1); subpedicelar and transmembranous isolated glomerular deposits of the immune complex type (1, complicated with microhematuria after donation). None of these glomerulopathies was demonstrated by LM, hence the use of EM and IM is essential for diagnosis.
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PMID:[A morphologic study of 103 kidneys donated for renal transplantation]. 251 71

Thirteen patients with peripheral neuropathy caused by necrotizing vasculitis were clinico-pathologically analyzed. These patients consisted of nine classical periarteritis nodosa (PN), four allergic granulomatous angitis (Churg-Strauss syndrome, AGA). All of them were proven to have a necrotizing vasculitis by sural nerve biopsy. The characteristics of peripheral neuropathy of these patients were summarized as follows. 1) Mononeuritis multiplex was a principal features in all patients preferentially localized in common peroneal, sural, radial median and ulnar nerves, with all modality of sensory impairment. 2) Radiation or diffuse deep-pain was a major initial symptom. Since this pain occurs frequently in the manner of sudden onset, the patient can tell the day of onset. 3) Local edema on the skin of involved region was initially observed. 4) Muscular atrophy and weakness was distributed more widely than sensory impairment. 5) Morphometric and teased-fiber study of biopsied sural nerves revealed axonal degeneration as a major pathological process. As compared to myelinated fibers, unmyelinated fibers were likely to be well preserved in morphology and population, which suggests that unmyelinated fibers are relatively resistant to ischemia. 6) Motor and sensory conduction study showed greatly decreased sensory and motor action potentials frequently resulting in absent of recordings. Conduction velocity is almost within normal range or just below the normal. Routine EMG recordings showed active denervation potentials in the involved muscles. 7) Protein in CSF was rarely elevated which suggested involvement of the spinal roots is infrequent. 8) Hypereosinophilia, thrombocythemia, fever, increased erythrocyte sedimentation rate, positive CRP and RA, and polyclonal hypergammaglobulinemia (IgG, IgA) were observed in most cases.
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PMID:[Clinical features of the peripheral nerve involvement in necrotizing angitis--characteristics in polyarteritis nodosa and allergic granulomatous angitis]. 256 7

Poly- and monoclonal antibodies to neoantigens of the human C5b-9 complement complex, as well as polyclonal antibodies to C5, C8, and C9, were used to detect and identify C5b-9 deposits in human myocardial tissue. Immunocytochemical studies were performed on fresh-frozen autopsy material derived from patients with myocardial infarctions; in addition, in 17 of these patients, paraffin sections of formalin-fixed tissue were investigated. Sixteen autopsies from patients with noncardiac diseases were analyzed as controls. Without exception, C5b-9 positivity was registered selectively and exclusively on and in myocardial cells located within the zones of infarction. The selectivity of staining was confirmed by control reactions for succinic dehydrogenase activity performed in adjacent, respective double-stained sections. Most intensive staining with anti-neoantigen antibodies was observed in the peripheral areas of the infarctions. Weak staining for C3d, rather strong staining for C5 and C9, and intermediate staining with anti-C8 antibodies were observed in the same localizations. Stainings for C4 and IgA were negative, whereas immunocytochemical reactions for IgG and IgM revealed an irregular and very weak staining. Only very weak staining was also observed with a monoclonal antibody to complement S-protein, indicating that the terminal complement components were deposited mainly in the form of membrane-damaging C5b-9 complexes. Immunocytochemical staining for C5b-9 was found to represent a most sensitive tool for detection of ischemic myocardial lesions, permitting easy detection even of single cell necroses. As a working hypothesis, we suggest that initial ischemia may cause loss of the ability of the heart muscle cells to regulate complement turnover at the membrane level. The resulting deposition of C5b-9 on the cell membranes may contribute to functional disturbance and irreversible damage of myocardial cells during the infarction process.
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PMID:Deposition of the terminal C5b-9 complement complex in infarcted areas of human myocardium. 352 91

Observations on early pathophysiology of burning suggests that the release of prostaglandins and thromboxanes plays a role in dermal ischemia. Because of the similarities of the early-phase frostbite wound, blister fluids were aspirated from 10 patients with frostbite, and routine biochemical analysis, immunoelectrophoresis, immunodiffusion, and evaluation of prostaglandins E2, F2 alpha, and thromboxane B2 were performed. Potassium, serum glutamic-oxaloacetic transaminase (SGOT), creatine phosphokinase (CPK), and lactic dehydrogenase (LDH) levels exceeded normal serum values. All blisters were found to have IgM, IgG, IgA, C3a, and opsonin. PgE2 was present in levels less than normal, but PgF2 alpha and TxB2 were markedly elevated. Since the vasoconstricting metabolites of arachidonic acid, PgF2 alpha and TxB2, are known to mediate dermal ischemia in burns and pedicle flaps, it is suggested they may play a role in the pathogenesis of frostbite.
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PMID:Evaluation of hand frostbite blister fluid as a clue to pathogenesis. 720 18

Cells infiltrating the nonsensory epithelium of the vomeronasal organ of virus-antibody-free rats exhibited surface immunoreactivity for beta 2-microglobulin and immunoglobulin (Ig) E. They were further characterized by using immunohistochemical techniques with antibodies to cell-specific markers or histochemical techniques for immunocytes with surface receptors for IgE. Localization of intracellular granules immunoreactive for lactoferrin and CD18, a leukocyte adhesion molecule, unequivocally identified these cells as neutrophils. The low number of IgA- and IgG-immunoreactive B lymphocytes, T lymphocytes, and accessory immunocytes in the vomeronasal organ as well as the rest of the nasal cavity confirmed the absence of infection. We hypothesize that the operation of the vomeronasal pump induces repeated episodes of transient focal ischemia followed by reperfusion, which results in release of neutrophil chemoattractants and modulation of adhesion factors that regulate the extravasation and migration of neutrophils into the nonsensory epithelium. The distribution of immunoreactivity for interleukin 8 suggests that it is not the primary neutrophil chemoattractant in this system while that of CD18 suggests its active involvement in neutrophil extravasation. In addition to their role in immune surveillance, neutrophils may stimulate ion/water secretion into the vomeronasal lumen, affecting the perireceptor processes regulating stimulus access and clearance from the sensory epithelium.
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PMID:Identification of neutrophils in the nonsensory epithelium of the vomeronasal organ in virus-antibody-free rats. 775 Jan 29

Necrotizing enterocolitis (NEC) is a devastating gastrointestinal disease of premature neonates that accounts for 3000 to 4000 deaths each year in the United States. The pathogenesis is not well understood, however theories suggest that prematurity, enteral feeding, bacterial colonization, and intestinal ischemia contribute to the intestinal injury. Furthermore, recent studies have shown that platelet activating factor and perhaps other inflammatory mediators mediate bowel necrosis in animals and possibly in humans. Although no specific intervention for NEC treatment exists, preventive therapy using either enteral IgA supplementation, breast milk feeding, antibiotic prophylaxis, or exogenous steroid administration have reduced the incidence of this overwhelming disease in small randomized trials. These modalities and perhaps PAF antagonists or other inflammatory mediator inhibitors may reduce the incidence or severity of NEC in the next several years.
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PMID:Necrotizing enterocolitis: a review of pathogenetic mechanisms and implications for prevention. 851 29

Autopsy records of 9 cases of neonate Hirschsprung's enterocolitis (HD) and 16 cases of neonate necrotizing enterocolitis (NEC) were analysed. It was found that the NEC lesions were more extensive than HD lesions, the bleeding and inflammation in NEC were also more serious than in HD. From our 21 animal experiments in which we tried to clarify the pathogenesis of Hirschsprung's enterocolitis and NEC, our preliminary hypothesis fro the development of Hirschsprung's enterocolitis being: the distal segment was first obstructed, causing the proximal segment to expand, the increase of pressure within the bowel resulted in ischemia of the intestines, increased bacterial multiplication in the retained feces and bacterial infiltration of the intestinal mucosa. The above being the major cause of HD. When the neonate is in asphyxia or shock, ischemia of the intestines and immunoallergic reactions occur, due to the lack of IgA in the mucosa, the multiplication and infiltration of pathogenic enterobacteria in the intestinal wall results in NEC.
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PMID:[A pathological comparison between Hirschsprung's enterocolitis and neonate necrotizing enterocolitis]. 874 74


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