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PubMed1993

[Changes in gastric mucosal glycosidases and thiobarbituric acid reactants induced by burn stress in obstructive jaundice rats].

To elucidate the pathogenesis of acute gastric mucosal lesion (AGML), burn stress was loaded in rats with and without obstructive jaundice. The activation of gastric mucosal glycosidases (beta-N-acetyl-D-glucosaminidase (NAG), beta-glucuronidase (BG)), which were released into the cytoplasm as a results of instability of the lysosomal membrane, was studied biochemically, enzymatically and histochemically after burn stress with and without obstructive jaundice. The latent enzyme activity calculated by NAG or BG, which represented the stability of lysosomal membrane, was lowest at 2-3 hour after burn stress in both groups. In other words, the degree of activation of the glycosidases was highest at 2-3 hour after burn stress. The latent enzyme activity calculated by NAG decreased significantly (p < 0.05) at 1 hour after burn stress in obstructive jaundice group compared with the non-obstructive jaundice group. The staining of NAG before burn stress was observed in mucus neck cell and surface epithelial cell in granular shape and it was observed diffusely after burn stress, especially in obstructive jaundice group. The changes in staining of BG was similar to NAG. Before activation of glycosidases, the thiobarbituric acid reactants, which are considered products of lipid peroxidation, increased promptly at 30 min after burn stress in both groups. Ulcer index increased gradually after burn stress and the significance was found between in the obstructive jaundice group and in non-obstructive jaundice group at 3 hour after burn stress. It's concluded that obstructive jaundice accelerated the fragility of lysosomal membrane after burn stress and these change were considered to be the reasons of frequent occurrence of AGML.

Acetylglucosaminidase↗
PubMed1984

Heterogeneous IgA glomerulonephropathy in liver cirrhosis.

Kidney and liver sections were obtained from 75 consecutive autopsy cases with liver cirrhosis discovered at post-mortem. Mesangial IgA as the predominant immunoglobulin was found in 36% (27) cases, with accompanying IgM in 10, and IgG in three subjects. IgA deposits occurred more frequently in micronodular cirrhosis than in macronodular and mixed types. There was no direct correlation with alcoholism or HBs antigen-orcein positivity in livers. The IgA antigen-antibody complexes formed against infectious and/or dietary antigens may bypass the liver phagocytic system via collateral shunts and cause the mesangial IgA deposits. IgA-bearing plasma cells in the liver (80%) may also contribute to the deposits. In cases of liver cirrhosis, there was a variable glomerular morphology including normal appearance by light microscopy (32%), minor changes (38.7%), diffuse mesangial sclerosis (12%), diffuse mesangial cell proliferation, and infrequently membranous and diffuse proliferative glomerulonephritis with a 'lobular pattern'. Five (6.7%) cases showed focal and segmental mesangiolysis with glomerular aneurysms, probably caused by toxic and/or infective agents bypassing the liver reticuloendothelial phagocytic system and acting on the mesangium to cause rupture of anchor points and formation of capillary aneurysms. The cirrhotic glomerulonephropathy was usually clinically latent, but two biopsy cases with mesangiocapillary glomerulonephritis had developed a nephrotic syndrome.

Adult↗
PubMed2002

A silver-free, single-sheet imaging medium based on acid amplification.

We describe a photographic medium that uses acid-amplified imaging (AAI) rather than silver halide development to amplify a latent image. The latent image is captured when small amounts of superacid are generated by the photolysis of iodonium salts sensitized by cationic dyes. During thermal processing, the quantity of acid is multiplied in a process catalyzed by strong acid, resulting in a much larger amount of a weaker acid. Acid-sensitive indicator dyes that diffuse into regions where acid has been produced form a colored image. The AAI system is not sufficiently sensitive for direct use in cameras but is suitable for many printing applications.

Journal Article↗
PubMedDate not supplied

[High prevalence of the Epstein-Barr virus in a Mexican population with Hodgkin's disease].

The Epstein-Barr virus (EBV) has been demonstrated in association with cases of Hodgkin's disease (HD) indicating that, in at least in some cases, EBV may play a pathogenic role in the development of HD. To determine the prevalence of EBV in HD in a Mexican adult population, we studied 39 formalin-fixed and/or B-5, paraffin embedded samples of patients with HD, by immunoperoxidase; in situ hybridization was done in 32 of the 39 cases. We analyzed the presence of the latent membrane protein (LMP) and EBV-specific DNA sequences. Reed-Sternberg cells and mononuclear variants were positive for LMP in 28 cases (72%). LMP staining was found both on the cell surface and/or within the cytoplasm with enhancement in the Golgi area. The LMP was found in the single case of diffuse lymphocyte predominant HD, in 6/12 cases of nodular sclerosis (50%), in 10/15 cases of mixed cellularity (67%) and in all eleven cases of lymphocyte depleted HD (100%). No EBV-specific DNA sequences were found by in situ hybridization. Our results show: 1) a higher association of EBV in our population compared to the approximately 48% reported in developed countries; 2) all histologic subtypes of HD in Mexico appear to be strongly associated with EBV in contrast to the strong association with only mixed cellularity seen in Western populations; 3) the high prevalence of EBV in HD in Mexico may be a function of histology, ethnic groups, socioeconomic factors and/or geography.

Adolescent↗
PubMed1989

Human immunodeficiency virus (HIV)-induced disease of the central nervous system: pathology and implications for pathogenesis.

Significant contributions from many different groups during the last 2 or 3 years have characterized relatively uniform neuropathological changes of the CNS in AIDS patients. They feature human immunodeficiency virus (HIV)-induced multinucleated giant cells as a histopathological hallmark and HIV demonstrable by electron microscopy, immunocytochemistry, and in situ hybridization. Unfortunately, a varying and confusing terminology is used to designate these changes which have been reported in surprisingly different incidences. Focal lesions have a microgranulomatous appearance and were designated as multifocal giant cell encephalitis or subacute encephalitis, which may be confused with the nodular encephalitis caused by cytomegalovirus. For some authors, the latter designation also covers characteristic diffuse white matter changes which have been termed progressive diffuse leukoencephalopathy by others, and which may overlap with focal lesions. Pathological features of these HIV-induced syndromes and other data do not support a major cytopathic effect of HIV on neural cells; rather, they suggest secondary pathogenetic events involving the predominant cell type in the lesion, the monocyte/macrophage/microglia. However, low-level, latent, and persisting HIV infections of neural cells cannot be excluded at present; the CNS may then serve as an early infected virus reservoir. A detailed correlation of clinical symptoms and stage of the infection to neuropathological changes is currently lacking but urgently needed. The presence of the HIV-receptor (CD4) molecule on brain cells is controversial; similarly, a putative cross-reaction of HIV proteins with trophic substances and transmitters needs to be substantiated.

Acquired Immunodeficiency Syndrome↗
PubMed2001

Epstein-Barr virus-positive aggressive lymphoma as a consequence of immunosuppression after multiple salvage treatments for follicular lymphoma.

We report on a patient with follicular non-Hodgkin's lymphoma (NHL) who developed a fatal high-grade Epstein-Barr virus (EBV)-positive NHL after conventional chemotherapies. The sudden onset of the high-grade lymphoma was accompanied by increasing circulating EBV genome copies and was complicated by spontaneous rupture of the spleen. Splenic tissue was diffusely infiltrated by large B cells. In situ hybridization for Epstein-Barr-encoded RNA (EBER) 1-2 was positive in 70% of cells, and molecular analysis revealed the presence of EBV DNA and a monoclonal IgH gene rearrangement. This case shows that the immunosuppression of multiple treatments may induce uncontrolled reactivation of a latent EBV infection, contributing to high-grade transformation in heavily treated lymphoma patients.

Adult↗
PubMed2000

The role of cytokines in the pathogenesis and management of AIDS-related lymphomas.

AIDS-related non-Hodgkin lymphomas (AIDS-NHL) consistently derive from B-cells and are characterized by extreme clinical aggressiveness. At histological level, AIDS-NHL are classified as AIDS-related Burkitt's lymphoma (AIDS-BL), AIDS-related diffuse large cell lymphoma (AIDS-DLCL) and AIDS-related primary effusion lymphoma (AIDS-PEL). The role of cytokines in the pathogenesis and management of AIDS-NHL has been studied to a certain extent. Production of large quantities of human IL-10 occurs frequently in AIDS-BL and correlates with latent EBV infection of the tumor clone. Lesser amounts of the cytokine are released in EBV negative cases. The pathogenetic role of IL-10 in AIDS-BL is suggested by the observation that IL-10 antisense oligonucleotides inhibit proliferation of the lymphoma. A significant fraction of AIDS-BL cell lines produce TNFbeta. Among AIDS-NHL, the release of TNFbeta appears to be specific for AIDS-BL. The pathogenetic relevance of TNFbeta in lymphomagenesis is suggested by the observation that some BL cell lines use TNFbeta as an autocrine growth factor. Some cases of AIDS-BL, particularly those carrying EBV infection, also secrete IL-6, IL-7 and IL-12. With respect to AIDS-DLCL, many cases express the IL-6R, rendering these cells responsive to the paracrine stimulation by the IL-6 produced by nearby T-cells, macrophages and endothelial cells which are frequently abundant in these tumor samples. The tumor clone itself, however, generally fails to release IL-6. AIDS-PEL is characterized by secretion of large amounts of IL-6 and IL-10. Some PEL cases also release oncostatin M. Apart from human IL-6, PEL also express viral IL-6, which is encoded by the HHV-8 genome. The biological relevance of both IL-6 and IL-10 in PEL proliferation and growth has been recently clarified in vitro and in vivo. Overall, these data suggest that activation of different cytokine loops clusters with different clinico-pathologic categories of AIDS-NHL and may represent the potential target of novel therapeutic strategies.

B-Lymphocytes↗
PubMed1975

Halothane on irradiated liver tissue.

The results of animal experiments show that distinction must be made between acute and chronic tissue changes produced by irradiation of the liver. The pathologico-morphological findings obtained by irradiation of the liver combined with repeated halothane administration during short-term experiments are scanty and dosage-dependent. Long-term observation has revealed higher-dosage irradiation to be followed by minor inflammation which, if combined with regular halothane administration, progresses to produce the patho-anatomical picture of chronic hepatitis with diffuse cell damage and focal necrosis even in those groups of animals which had been exposed to low-dosage irradiation. It must be assumed that even low-dosage irradiation of the liver which fails to produce measurable changes at the beginning, may influence the structure and function of the hepatic parenchyma. The latent radiation damage manifests itself under additional toxic irritation of the liver, such as that caused by halothane.

Acute Disease↗
PubMed1989

[Thyroid microsomal autoantibodies in thyroid disease: their value as an antigenic marker].

An autoimmune disease can be the cause of thyroid disfunction. Determination of autoantibodies titers is the best way of demonstrating its existence. We studied 172 thyroid patients (146 females, 26 males) with ages ranging from 15 to 81 years. Thyroid microsomal autoantibodies (TMA) were detected by a modified agglutination test (SERA-TEK kit, Ames Div); a dilution greater than or equal to 1/1600 was considered as diagnostic of autoimmune disease. Patients were classified according to morphological and functional status in 3 groups: GI = non toxic goiter, n = 98 (71 diffuse, 20 multi and 7 uninodular); GII = toxic goiter, n = 62 (52 diffuse, 4 multi, 2 uninodular and 4 subacute thyroiditis); G III = hypothyroidism, n = 12 (5 primary hypothyroidism and 7 chronic thyroiditis). A control group of 30 normal individuals, ages ranging from 19 to 85 years was also studied. Diagnostic titers of TMA were found in 30.8% of group I, 88.5% of group II, 91.6% of group III and only in 6.6% of controls. The high incidence of positive TMA in toxic diffuse goiter (96.1%) as well as in hypothyroid patients was expected since these are typical examples of thyroid autoimmune disease. In the non toxic goiter group, positive TMA were present in 50% of multinodular, 28% of uninodular and 25% of diffuse goiters and the incidence of positive TMA varied according to age, being higher over the age of 40 years and lower under the age of 20 years. We postulate that this unexpected high incidence of positive TMA in non toxic goiter is due to amelioration of chronic iodine deficiency inducing the expression of latent autoimmune disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2006

Genetic association analysis of functional impairment in chronic obstructive pulmonary disease.

RATIONALE: Patients with severe chronic obstructive pulmonary disease (COPD) may have varying levels of disability despite similar levels of lung function. This variation may reflect different COPD subtypes, which may have different genetic predispositions. OBJECTIVES: To identify genetic associations for COPD-related phenotypes, including measures of exercise capacity, pulmonary function, and respiratory symptoms. METHODS: In 304 subjects from the National Emphysema Treatment Trial, we genotyped 80 markers in 22 positional and/or biologically plausible candidate genes. Regression models were used to test for association, using a test-replication approach to guard against false-positive results. For significant associations, effect estimates were recalculated using the entire cohort. Positive associations with dyspnea were confirmed in families from the Boston Early-Onset COPD Study. RESULTS: The test-replication approach identified four genes-microsomal epoxide hydrolase (EPHX1), latent transforming growth factor-beta binding protein-4 (LTBP4), surfactant protein B (SFTPB), and transforming growth factor-beta1 (TGFB1)-that were associated with COPD-related phenotypes. In all subjects, single-nucleotide polymorphisms (SNPs) in EPHX1 (p < or = 0.03) and in LTBP4 (p < or = 0.03) were associated with maximal output on cardiopulmonary exercise testing. Markers in LTBP4 (p < or = 0.05) and SFTPB (p = 0.005) were associated with 6-min walk test distance. SNPs in EPHX1 were associated with carbon monoxide diffusing capacity (p < or = 0.04). Three SNPs in TGFB1 were associated with dyspnea (p < or = 0.002), one of which replicated in the family study (p = 0.02). CONCLUSIONS: Polymorphisms in several genes seem to be associated with COPD-related traits other than FEV(1). These associations may identify genes in pathways important for COPD pathogenesis.

Aged↗
PubMed1975

Fatal disseminated adenovirus infection in a renal transplant recipient.

A 61 year old woman died of diffuse interstitial adenovirus pneumonia 55 days after receiving a cadaveric renal allograft. The adenovirus was serologically distinct from the 33 known human adenovirus serotypes and appears to represent a new human adenovirus. Pathologic and virological findings indicate that the pneumonia was only one manifestation of a disseminated infection, the source of which may have been a latent adenovirus infection preexisting in the donor kidney. The establishment of the etiologic diagnosis in this case, which was complicated by the presence of oculocutaneous and esophageal herpes simplex virus infection as well as focal pulmonary aspergillosis, required coordinated histopathologic and virological investigation. Our findings demonstrate that severe viral infections in transplant recipients are not caused exclusively by members of the herpesvirus group.

Adenoviridae↗
PubMed2005

A prognostic approach to defining chronic pain.

This paper develops a prognostic approach to defining chronic back pain. Possible and probable chronic back pain were defined, respectively, by a 50% and an 80% (or greater) probability of future clinically significant back pain. We assessed whether an empirically derived chronic pain classification satisfied these validating criteria among 1213 primary care back pain patients assessed at baseline and at 1, 2 and 5 year follow-ups. From multiple measures of back pain intensity and dysfunction, Latent Transition Regression Analysis empirically identified four pain severity latent classes: no pain; mild pain; moderate pain and limitation; and severe, limiting pain. From one observation point to the next, patients were most likely to remain in the same pain severity class, but chronic pain was better characterized as a dynamic state than a static trait. Among persons with severe, limiting pain, prognostic variables (depression, diffuse pain, pain persistence) improved prediction of future severe, limiting pain. A risk score developed from pain severity and prognostic measures identified risk levels corresponding to 50 and 80% probability thresholds for predicting future clinically significant back pain. At baseline and 1 year, 6.1 and 4.4% of study patients met or exceeded the 80% risk threshold for probable chronic back pain. An additional 20.3% at baseline and 12.5% at 1 year met or exceeded the 50% risk threshold for possible chronic back pain. Defining chronic pain prospectively, by risk thresholds for future clinically significant pain, provides an empirically grounded approach to chronic pain assessment.

Adolescent↗
PubMed1976

[Decrease in efficiency after experimental virus encephalitis. Small scale experimental tests on mice and histologic evaluation (author's transl)].

Two different experiments were set up in order to test the efficiency of 281 mice which had been infected intracerebrally with yellow fever virus 17 D of various dilutions (10(-1)-10(-5)); the tests were run after two time periods (40--55 days after infection = I. date, and 97 and 160 days after infection = II. date). In the first experimental set-up the animals were to find their food in a labyrinth- after 24 hours without food, (Labyrinth Experiment, Fig. 1). The time was taken from the moment when the mouse was put into the cage until the moment when it ate from the food. 4.37 min, were considered to be "standard time". In the second experiment the mice were placed on a horizontal rod rotating round an axle (Rotating Rod Experiment, Fig. 2 a,b,c). The time was measured for how long the animals could stay on the rod. 90/10 sec., were ascertained as "standard time". The following results were obtained. The difference in time regarding the I. and II. date is clearly noticed by the experiment with the rotating rod. The performance time of the animals was almost doubled after the 2nd time period (Table 4a and b, Fig. 3a and b), i.e. the animals could stay on the rod almost twice as long as after the first time period, which means that the recovery process of the animals can be measured by means of the rod experiment. In this respect the experiment with the labyrinth is less suitable. The recovery of the animals as well as the residual damages depended on the inoculated virus dilutions (Table 5a and b, Fig. 4a and b, Tables 7 and 8, Fig 21a and b). The histologic findings of the animals show lesions in all regions of the Central Nerve System (Fig 6-20, Table 2). The deficiencies of the animals which are due to diffuse damages of the Central Nerve System are demonstrated by the rotating rod experiment, whereas the labyrinth experiment verifies the shortcomings of the cornu ammonis (olfactory brain). The rotating rod experiment is the more sensitive of the two models as the majority of the lesions are distributed diffusely on the Central Nervous System. The severe lesions of the Central Nerve System which are supported by histologic findings - even 160 days after infection, are confirmed by the deficiencies in the performance processes of the animals (delayed damages). Discussion have taken place regarding whether the experimental results of the animals can be applied to assessing latent or delayed damages in children after an encephalitis. The latter could concern in how far the course of an encephalitis depends on the originating virus dosis and could also relate to the development of delayed damages. The knowledge regarding the formation of delayed damages, their assessment as well as the prevention of encephalitis in infants would thus be greatly improved. In order to judge therapeutic measures on animals the rotating rod experiment appears to be very suitable since each stage of the illness enables an assessment of the state of the disease.

Animals↗
PubMed1998

Subcellular localization of (latent) transforming growth factor beta and the latent TGF-beta binding protein in rat hepatocytes and hepatic stellate cells.

Recently, the existence of the large latent transforming growth factor beta (TGF-beta) complex, consisting of TGF-beta, the N-terminal part of its precursor (latency-associated peptide [LAP]), and the latent TGF-beta binding protein (LTBP), was demonstrated in rat liver parenchymal cells (PC) and stellate cells (HSC). However, in contrast to HSC, in freshly isolated PC, no message of these proteins is detectable. This study was performed to investigate the subcellular distribution of the proteins forming the latent TGF-beta complex in PC and HSC from rat liver to obtain more information about their origin and potential intracellular functions. PC and HSC were isolated from rat liver by protease reperfusion and investigated for TGF-beta1,-2,-3, beta1-LAP, and LTBP-1 after cultivation using double-immunofluorescent staining, followed by high-resolution confocal microscopic analysis. Subcellular fractions obtained by standard differential centrifugation of rat liver homogenate were analyzed using a TGF-beta1 enzyme-linked immunosorbent assay (ELISA) and Western blotting for beta1-LAP and LTBP-1. By confocal microscopy, a diffuse distribution of TGF-beta and LAP in the cytoplasm of PC is noticed, whereas the LTBP immunostaining predominates at plasma membranes. In PC, distinct intracellular granules were superimposed with TGF-beta, LAP, and LTBP stainings identified as lysosomal compartments and mitochondria by ELISA and immunoblotting of subcellular fractions. In HSC, stainings of colocalized TGF-beta, LAP, and LTBP are strongest in the perinuclear area, indicating synthesis and secretion via endoplasmic reticulum and Golgi, respectively. Partially, the proteins were also found in HSC nuclei. During the transformation of HSC to myofibroblasts, LAP and LTBP become strongly colocalized with other components of the cytoskeletal network like smooth muscle--actin, desmin, and talin. The results confirm biochemical data about the existence and expression of the large latent TGF-beta complex in PC and HSC, respectively. Baseline information is provided from which new hypotheses regarding intracellular functions of TGF-beta, LAP, and LTBP in liver parenchymal and stellate cells can be concluded.

Animals↗
PubMed2002

Latent cerebral hypoperfusion in a boy with persistent nephrotic syndrome.

Pediatricians are often faced with both bad temper and decreased daily activity in children with persistent nephrotic syndrome. These problems, which might affect both mental and physical development, have been explained as a consequence of general fatigue due to systemic edema and/or long-term hospitalization. However, other factors, such as cerebral hypoperfusion, may be involved. We experienced a case of a boy with steroid-resistant nephrotic syndrome who showed diffuse cerebral hypoperfusion on single photon emission computed tomography. Diffuse cerebral hypoperfusion dramatically resolved as the nephrotic syndrome remitted. His bad temper, decreased daily activity, and delay of speech and motor development also improved. In our patient, cerebral hypoperfusion might have been associated with his mental problems, physical problems, and delayed development of speech.

Cerebral Cortex↗
PubMed1999

Dissemination of latent colon adenocarcinoma after laparoscopic cholecystectomy.

The seeding of neoplasms at trocar sites has been reported with increasing frequency. A case is presented of a 68 year-old woman with metastatic seeding of nondiagnosed colon cancer at the umbilical trocar site used for a laparoscopic cholecystectomy. Histopathological examination showed metastatic adenocarcinoma probably of gastrointestinal origin. A colonoscopy performed at the same time revealed a 2-cm lesion at the hepatic flexure which was shown histologically to be a differentiated adenocarcinoma. Diffuse peritoneal carcinomatosis was also found on computerised tomography. It is presumed that the primary colon cancer existed prior to cholecystectomy.

Adenocarcinoma↗
PubMed1993

Does gastric adenocarcinoma develop after the treatment of gastric lymphoma?

Two adult patients with the diagnosis of gastric lymphoma who developed adenocarcinoma of the stomach 8 years after the treatment are presented. Both patients were treated by subtotal gastrectomy followed by irradiation of 4,000-4,500 cGy to the epigastric region and six courses of chemotherapy (vincristine, cyclophosphamide, prednisolone). In our review of the literature, 16 cases of gastric adenocarcinoma following the treatment of gastric lymphoma were found and listed with details. The factors influencing the development of this secondary carcinoma, mainly those treatment related are discussed. The possible role of both radiotherapy and chemotherapy in shortening the latent period for the development of stump carcinoma is emphasized.

Adenocarcinoma↗