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At least 793 records · Page 44Linked to original sources
PubMed1976

Terminal deoxynucleotidyl transferase activities in human blood leukocytes and lymphoblast cell lines: high levels in lymphoblast cell lines and in blast cells of some patients with chronic myelogenous leukemia in acute phase.

Terminal deoxynucleotidyl transferase, an enzyme which catalyzes the polymerization of deoxyribonucleoside triphosphates, elongating oligo- or polydeoxynucleotide chains, but without direction from a nucleic acid template, is thought to be specific for thymus gland and thymus-derived cells. We have confirmed the observations that high levels are characteristic of thymus gland with both human and calf tissue and that elevated levels may be found in some cases of acute lymphocytic leukemia. High levels were also found in human lymphoblast cell lines with T-cell characteristics, and insignificant activity was observed in leukocytes of patients with chronic myelogenous leukemia not in acute blast phase of the disease, chronic lymphocytic leukemia, human B-cells, and normal human blood lymphocytes even after stimulation with phytohemagglutinin. However, high levels (approximately 200 nmoles/hr/10(9) cells) equivalent to those in thymus tissue and lymphoblast cell lines with T-cell characteristics were found in the peripheral blood blast cells of four patients with chronic myelogenous leukemia in an acute blast phase of their disease. One hypothesis that may explain the present results is that in chronic myelogenous leukemia in acute blast phase of the disease the proliferative blast response may not always be myeloblasts but in some cases it may be lymphoblasts.

Adult↗
PubMed1979

Assessment of the value of thymic scan in myasthenia gravis.

Fifty-three patients were investigated by Se methionine scan in order to evaluate the role of the thymus gland in myasthenia gravis. The thymus of 28 of the above patients was examined histologically. Five out of six thymomas were detected with this technique and eight out of twelve hyperplasias were revealed. The above data suggests that Se methionine scan is a useful, innocuous tool for diagnosing neoplasms and abnormal germinal centers in thymus glands.

Adolescent↗
PubMed2001

[An immunopathological study of autoimmune keratitis in nude mice with embryonic rat thymus grafts].

PURPOSE: The purpose of the present study was to examine the keratitis detected in these mice after the xenogeneic thymus gland transplantation. METHODS: The thymus glands were collected from F 344 rat embryos and transplanted under the renal capsules of BALB/c nude mice (rat TG nude mice). Histological and immunohistological examinations and a transfer experiment of keratitis was also conducted. RESULTS: The histological image was characterized by the infiltration of mononuclear cells and neutrophils and the marked angiogenesis. The autoantibodies reacting specifically to corneal epithelial cells and corneal stroma were recognized in the blood. The deposits of immunoglobulins and complements were simultaneously observed in the corneal stroma and around the basement membrane. Corneal lesions of rat TG nude mice were therefore successfully transferred into naive nude mice by host splenic CD 4 positive cells. CONCLUSION: The present study demonstrated that autoimmunity was involved in the development of keratitis in rat TG nude mice and that these mice were the first animal models to develop autoimmune keratitis spontaneously.

Animals↗
PubMed1978

Comparison of effects of dietary T-2 toxin on growth, immunogenic organs, antibody formation, and pathologic changes in turkeys and chickens.

The effect of T-2 toxin (trichothecene mycotoxin) consumption on Broad-Breasted White turkey poults and White Leghorn chicks was studied. Groups of ten 8-day-old poults were fed rations containing T-2 at 10 ppm, 2ppm, or 0 ppm (controls) for a period of 4 weeks; a 4th group (inanition control) was fed control rations equal to the amount consumed by the group fed rations containing T-2 at 10 ppm during the previous 24 hours. A similar experimental design was used to study the effect of the toxin on 1-day-old chicks. The thymus glands of the poults given the feed containing 10 ppm were markedly decreased in size compared with thymus glands from poults in the control group, 0.182 vs 0.331 (percentage of body weight). There was no significant (P less than or equal to 0.05) decrease in thymus gland size in poults given 2 ppm or in the inanition controls. Dietary treatment did not appear to affect the size of the bursa or spleen of the poults. Histopathologic examination of thymus glands from poults given 10 ppm of T-2 revealed a depletion of cortical lymphocytes. Chicks appeared less sensitive to T-2 toxin than did the poults. There was no effect by any dietary treatment on the size of the thymus gland, bursa, or spleen of chicks. Reductions were noticed in feed efficiency and weight gain. There was no effect of T-2 toxin on agglutinating antibody formation to Pasteurella multocida bacterin.

Animals↗
PubMed1976

[Atrophy of adrenal gland and thymus following cortisol treatment in newborn rats (author's transl)].

Effects of neonatal treatment with cortisol on the mortality, growth rate, the weight of thymus, spleen and adrenal gland, blood lymphocyte counts and stress responses were examined in the rat. In rats treated with 1 mg cortisol the survival rate was only 13 percent, and in those given 0.75 mg the rate was 47 percent. Large doses of cortisol produced "wasting syndrome" and the animals died during a period from 5 to 13 days after the injection. Over the first week the body weight did not increase in rats injected with cortisol in doses of 1 and 0.75 mg. A marked atrophy of the thymus and a great reduction of the blood lymphocyte counts were observed in rats treated with large doses of cortisol. The development of spleen was temporarily inhibited. The adrenal gland was remarkably atrophied: the gland weight at 21 days of age was similar to that at birth and only 22 percent of the control value. In rats injected with 0.5 mg cortisol plasma corticosterone response to ether inhalation was not different from that of normal controls at 21 days of age. However, rats treated with 0.75 and 1 mg cortisol did not show plasma corticosterone response on exposure to a strange environment. The effect of several kinds of corticoids was also examined. Dexamethasone and betamethasone caused a marked atrophy of the thymus and spleen. Cortisol and deoxycorticosterone produced a large decrease in the adrenal corticosterone content. The effect of exogenous corticosterone was less in extent as compared with that of cortisol.

Adrenal Glands↗
PubMed1987

Possible association of thymus dysfunction with fading syndromes in puppies and kittens.

"Wasting" or "fading" syndromes are common causes of puppy and kitten mortality. Numerous infectious and toxic, metabolic, or nutritional factors could potentially be responsible for wasting and death in young animals. Evidence has been presented that infectious canine hepatitis virus infection, beta-hemolytic streptococcus infection, and feline infectious peritonitis virus infection are responsible for a significant number of deaths due to wasting syndrome. However, many cases of wasting syndrome cannot be attributed to infectious agents or other specific etiologies. The thymus gland warrants special attention when one is evaluating an animal with a wasting syndrome because it is known that, in some species, neonatal thymectomy results in wasting and death. Unfortunately, most reports describing fading syndromes in puppies and kittens do not mention the gross or histologic appearance of the thymus gland at postmortem examination. When examining the thymus gland, one must keep in mind that the thymus may be hypoplastic owing to a congenital or genetic defect in its structure and function or it may be atrophic secondary to whatever is causing the fading syndrome. If a thorough history, clinical examination, and/or postmortem examination do not reveal a cause for the fading syndrome, then defective thymus function should be considered as a possible causative or contributing factor to the fading syndrome. In these cases, therapy designed to replace or improve the defective thymus function should be considered. At least one form of wasting syndrome in puppies (immunodeficient dwarfism) has been found to respond to short-term therapy with a thymus hormone (thymosin fraction 5) or with bovine growth hormone (which is thymotropic) in limited clinical trials. It is possible that other forms of wasting or fading syndromes would also respond to therapy with thymus hormone or growth hormone. Certain thymus hormones (thymopoietin pentapeptide, thymosin alpha 1, facteur thymique serique, and rabbit thymus acetone powder) and bovine growth hormone are commercially available. Before initiating therapy, one should consider that if the cause of the wasting syndrome is genetic, then successful treatment may perpetuate a genetic defect. More research (both basic and clinical) is needed to determine the role of thymus gland dysfunction in fading syndromes of puppies and kittens and if therapy with one or several of the thymus hormones or with growth hormone could reverse the symptoms of wasting.

Animals↗
PubMedDate not supplied

Epithelial framework reorganization during human thymus involution.

BACKGROUND: The thymus undergoes age-related (physiological) involution in the course of normal ontogenetic development. In addition to this chronic involution, the thymus can also undergo an acute (age-independent) regression, defined as spontaneous, transient involution. This process is induced by either exogenous or endogenous factors, including some infections (infection-type involution). OBJECTIVE: The purpose of the present work was to undertake a comparative study of the epithelial framework organization and cytokeratin immunoreactivity of human thymic epithelial cells during age-related and infection-induced involution. METHODS: Routine methods for light and transmission electron microscopy, as well as indirect immunoperoxidase staining and immunogold electron microscopy, were applied. RESULTS: The epithelial thymocyte microenvironment was of a generally similar cellular composition in both chronically and acutely involuted thymus. Structurally, aged thymus glands and infection-affected thymus glands displayed a large mass of adipose tissue containing scattered islands composed of epithelial cells, lymphocytes and reticular connective tissue. Correlation between thymus involution and regional peculiarities in the presence and distribution of cytokeratin-immunopositive cells and their intermediate filaments was investigated. CONCLUSION: The epithelial framework of the thymus undergoes reorganization during both age-related and infection-induced thymus involution. The involutionary processes demonstrated essential regional and intracellular (structural and immunocytochemical) differences. The epithelial cell rearrangement and cytokeratin modulation that we observed might be involved in thymic microenvironment plasticity and reorganization in the course of these processes.

Adolescent↗
PubMed1996

Study of the post-natal effects of chemopreventive agents on ethylnitrosourea-induced transplacental carcinogenesis in rats. II. Influence of low-molecular-weight polypeptide factors from the thymus, pineal gland, bone marrow, anterior hypothalamus, brain cortex and brain white substance.

The influence of the polypeptide factors extracted from thymus, pineal gland, bone marrow, anterior hypothalamus, brain cortex or brain white substance on N-ethyl-N-nitrosourea (ENU)-induced transplacental carcinogenesis was studied in rats. ENU was given to pregnant rats as a single i.v. exposure at a dose of 75 mg/kg body weight on the 21st day of gestation. The polypeptide factors were given to the offspring as a series of s.c. injections, at a dose of 0.5 mg/rat/day, starting at one or 2.5 months of age and continuing throughout the whole of post-natal life. ENU induced tumors of the brain, spinal cord, peripheral nerves and kidneys in 94-98% of the offspring exposed to the carcinogen, with an average number of 2.3-2.6 tumors per rat, and an average survival time of 294 days. Post-natal thymus factor or pineal gland factor administration was followed by an increase in mean lifespan of approximately 2 months and a significant decrease (P < 0.05) in the total tumor number per tumor-bearing rat, as well as the incidence and multiplicity of spinal cord tumors. Pineal gland factor also decreased the incidence of peripheral nerve and kidney tumors and their number per tumor-bearing rat. Brain cortex factor and brain white substance factor treatment was followed by a decrease in total tumor multiplicity of 1.2- to 3.3-fold, and a decrease in incidence of brain tumors of 10 to 33% per rat in comparison to the controls. Brain cortex factor also decreased the total tumor incidence. At the same time, brain white substance factor administration increased the incidence of peripheral nerve tumors and decreased the mean lifespan. Both bone marrow factor and anterior hypothalamus factor did not have any modifying effects on any of the ENU-induced tumors and mean lifespan. Thus, our results show the possibility of attenuation of transplacental ENU-induced carcinogenesis with post-natal administration of some polypeptide substances.

Animals↗
PubMed2003

CRP-ductin, the mouse homologue of gp-340/deleted in malignant brain tumors 1 (DMBT1), binds gram-positive and gram-negative bacteria and interacts with lung surfactant protein D.

CRP-ductin is a protein expressed mainly by mucosal epithelial cells in the mouse. Sequence homologies indicate that CRP-ductin is the mouse homologue of human gp-340, a glycoprotein that agglutinates microorganisms and binds the lung mucosal collectin surfactant protein-D (SP-D). Here we report that purified CRP-ductin binds human SP-D in a calcium-dependent manner and that the binding is not inhibited by maltose. The same properties have previously been observed for gp-340 binding of SP-D. CRP-ductin also showed calcium-dependent binding to both gram-positive and -negative bacteria. A polyclonal antibody raised against gp-340 reacted specifically with CRP-ductin in Western blots. Immunoreactivity to CRP-ductin was found in the exocrine pancreas, in epithelial cells throughout the gastrointestinal tract and in the parotid ducts. A panel of RNA preparations from mouse tissues was screened for CRP-ductin and SP-D expression by reverse transcription-PCR. The pancreas was the main site of synthesis of CRP-ductin, but transcripts were also readily amplified from salivary gland, the gastrointestinal tract, liver, testis, uterus and lung. Lung was the main site of synthesis of SP-D, but transcripts were also amplified from uterus, salivary gland, thymus, thyroid gland, pancreas and testis. We conclude that CRP-ductin is the mouse homologue of human gp-340 and that its capacity to bind SP-D as well as gram-negative and gram-positive bacteria suggests a role in mucosal immune defense.

Agglutinins↗
PubMed1995

Immunolocalization of a gonadotropin-releasing hormone receptor site in murine endometrium that mediates apoptosis.

Circumstantial evidence from a previous study indicated that antibodies generated against a synthetic N-terminal extracellular domain mouse pituitary gonadotropin-releasing hormone (GnRH) receptor peptide acted directly on the murine uterus affecting endometrial regression. Affinity-purified polyclonal sheep antibodies were used to assess tissue-specificity of antibody reactions in diestrous mice. Antibody binding was localized by immunofluorescence staining to anterior pituitary gland and endometrium. Ovary, brain, liver, kidneys, heart, lungs, spleen, gastrointestinal tract, adrenal glands, thymus, thyroid gland, muscle, and adipose were unreactive. Fragmented deoxyribonucleic acid, a marker of programmed cell death/apoptosis, was detected by digoxigenin labeling-immunoperoxidase in endometrial (but not pituitary) glands of animals injected with antipeptide antibodies or native ligand. It appears that luteal phase endometrium of mice expresses a GnRH receptor moiety that is coupled to a cell death (endonuclease) transduction pathway.

Amino Acid Sequence↗
PubMed2006

Estimation of radiation exposure in low-dose multislice computed tomography of the heart and comparison with a calculation program.

The purpose of this study was to evaluate the achievable organ dose savings in low-dose multislice computed tomography (MSCT) of the heart using different tube voltages (80 kVp, 100 kVp, 120 kVp) and compare it with calculated values. A female Alderson-Rando phantom was equipped with thermoluminescent dosimeters (TLDs) in five different positions to assess the mean doses within representative organs (thyroid gland, thymus, oesophagus, pancreas, liver). Radiation exposure was performed on a 16-row MSCT scanner with six different routine scan protocols: a 120-kV and a 100-kV CT angiography (CTA) protocol with the same collimation, two 120-kV Ca-scoring (CS) protocols with different collimations and two 80-kV CS protocols with the same collimation as the 120-kV CS protocols. Each scan protocol was repeated five times. The measured dose values for the organs were compared with the values calculated by a commercially available computer program. Directly irradiated organs, such as the esophagus, received doses of 34.7 mSv (CTA 16x0.75 120 kVp), 21.9 mSv (CTA 16x0.75 100 kVp) and 4.96 mSv (CS score 12x1.5 80 kVp), the thyroid as an organ receiving only scattered radiation collected organ doses of 2.98 mSv (CTA 16x0.75 120 kVp), 1.97 mSv (CTA 16x0.75 100 kVp) and 0.58 mSv (CS score 12x1.5 80 kVp). The measured relative organ dose reductions from standard to low-kV protocols ranged from 30.9% to 55.9% and were statistically significant (P<0.05). The comparison with the calculated organ doses showed that the calculation program can predict the relative dose reduction of cardiac low photon-energy protocols precisely.

Coronary Angiography↗
PubMed2003

Selective fetal hypophysectomy in utero: microsurgical technique and comparisons with hypophysectomy by decapitation.

A detailed description is given of a surgical technique for selectively removing the pituitary anlage from the intrauterine fetal rat as an alternative to the more generally applied fetal hypophysectomy by decapitation. Fetuses on the 17th day of gestation were approached through a narrow opening in the uterine wall and fetal membranes. The pituitary gland was sucked out with a fine glass tube introduced from the side of the head into the space between the pons and the ventral hypothalamus, where the gland is situated. The female rat was sacrificed on the 22nd day of gestation (the day before delivery) and the surviving fetuses were preserved. On average, 20% of the operated fetuses survived until that day, 20% of which were completely hypophysectomized (microscopical examination). Operated fetuses with intact pituitaries served as surgical controls for the evaluation of selected effects of the total hypophysectomy. Initial comparisons were made with published results based on hypophysectomy by decapitation, evaluated without access to surgical controls. The two methods of fetal pituitary removal provide consistent results as regards the weight increase of adrenal and thyroid glands (retardation), thymus gland (stimulation) and testicles (no effect). On the other hand, body weight increase was not affected by selective hypophysectomy but instead slowed down after decapitation, whereas the growth in length of the humerus bone was stimulated and retarded, respectively.

Animals↗
PubMed1997

Expression of the putative transcription factor NOR-1 in the nervous, the endocrine and the immune systems and the developing brain of the rat.

NOR-1 is a novel member of the NGFI-B/RNR-1 subfamily within the nuclear receptor superfamily, and has been implicated in signal transduction mediated by various second messengers. To investigate the physiological role of NOR-1, we examined its gene expression in various adult rat tissues and developing rat brain by the quantitative reverse transcription-polymerase chain reaction using in vitro synthesized RNA as an internal standard. The NOR-1 gene was expressed in all tissues examined, but predominantly in the cerebral cortex and pituitary glands. Thymus, adrenal glands, spleen, epididymis, submandibular glands and deferent ducts showed moderate expression. In the brain, NOR-1 gene expression was developmentally regulated, with the peak levels on gestational day 18. These findings suggest a ubiquitous role of NOR-1 in signal transduction in diverse tissues. These findings also suggest that the nervous, endocrine and immune systems may be highly exposed to NOR-1-inducing stimuli under normal conditions in adult rats. Developing rat brain cells may most frequently receive the relevant signal on day 18 of gestation.

Animals↗
PubMed2001

Production of colony-stimulating factors and IL-5 by organs from three types of mice with inflammatory disease due to loss of the suppressor of cytokine signaling-1.

Organs from neonatal mice dying from IFN-gamma-dependent inflammatory disease initiated by loss of the gene encoding the suppressor of cytokine signaling-1 (SOCS-1) had a normal capacity to produce G-CSF in vitro but a reduced capacity to produce GM-CSF, most evident with the lung, and some reduction in the production of M-CSF by muscle tissue. In contrast, organs from mice lacking the genes for both SOCS-1 and IFN-gamma had a normal capacity to produce CSFs. Organs from young adult mice dying with polymyositis and myocarditis that lacked SOCS-1 but were heterozygous for IFN-gamma had a normal capacity to produce GM-CSF and M-CSF, but muscle tissue produced significantly increased amounts of G-CSF and IL-5 with IL-5 production also being elevated for the salivary gland, thymus, and heart. Loss of the IFN-gamma gene alone had no impact on organ production of these cytokines in vitro. In none of the inflammatory disease models was IL-3 production detected. The SOCS-1 protein appears to have no direct influence on the cellular production of these cytokines and the abnormalities observed either depend on the coaction of IFN-gamma, or more likely, are linked with the invasion and destruction of tissue by T lymphocytes, macrophages, eosinophils, and neutrophils. The ability of local organs to produce these proinflammatory cytokines could contribute to the development and progression of these inflammatory lesions.

Animals↗
PubMed1968

Organ weights and water content of rats fed protein-deficient diets.

To provide the basic information needed for studies of drug toxicity in rats suffering from protein deficiency, weanling male albino rats were fed for 28 days on either laboratory chow or a synthetic diet containing 27% or 8% of casein. The low-protein diet produced a kwashiorkoric cachexia characterized by stunting, alopecia, tail dermatitis, apathy, augmented calorie intake per kg body-weight and a 20% death rate. Autopsies at weekly intervals disclosed that the synthetic normal-protein diet produced a slight loss of total body-weight, due to loss of weight in the adrenal glands and gastrointestinal tissues, and a more-or-less generalized dehydration of body organs. The body-weight of the kwashiorkoric rats was half that of the control groups, due especially to loss of weight in caecum, kidneys, liver, muscle, skin, spleen, salivary glands and thymus gland; loss of weight was less marked in other organs, particularly the stomach, heart and testes and, especially, the brain. There was further dehydration of adrenals and brain but the liver and gastrointestinal tissues tended to be hydrated. The kwashiorkoric diet had not entirely suppressed growth-stimulated relative increase in weight of muscle, skin and testes. The histology of organs was essentially normal in the survivors. Absence of oedema in organs distinguished the kwashiorkoric rats from rats with total calorie depletion.

Animal Nutritional Physiological Phenomena↗