Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0011570 (
depression
)
172,036
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Experiments were performed on 12-wk-old nonobese diabetic (NOD) mice to investigate the immunologic background of the condition, using ICR mice as controls. The results indicate the following: (1) absolute decreases in number of T lymphocytes, (2)
depression
of natural killer activity, (3) normal responsiveness in delayed type hypersensitivity and functional
depression
of killer T cells against allogeneic tumors, (4) diminished resistance to
herpes
virus infection, and (5) enhanced production of polyclonal antibodies to T cell-dependent antigens. These features are similar to those noted in other autoimmune diseases of man and in their experimental models in laboratory animals. Elucidation of the pathogenetic mechanism of autoimmune diabetes mellitus in NOD mice, therefore, may contribute to the diagnosis, treatment, and prevention of a wide variety of autoimmune diseases.
...
PMID:Immunologic aspects of the nonobese diabetic (NOD) mouse. Abnormalities of cellular immunity. 629 42
The authors report the case of a 46-year old patient who died from fulminant herpetic hepatitis. No cause of immuno-
depression
was documented in this patient. No skin or mucosal herpetic lesion was found except a questionable urethritis.
Herpes
virus was demonstrated in the hepatocytes by electron microscopy and isolated from the serum. It was identified as
herpes
virus hominis type II. The low titer of circulating antibodies did not permit the distinction between herpetic primo-infection and reactivation. The features of the hepatic injury are discussed and compared with previous reports. An active diagnostic approach of herpetic hepatitis is considered.
...
PMID:[Fatal herpetic hepatitis in an apparently healthy adult]. 630 98
The current study examined how individuals deal with genital herpes, a recurrent, incurable disease with a great psychological impact. An assessment battery composed of cognitive and problem-focused coping, attribution, and social support mechanisms was employed. These coping mechanisms were correlated with measures of psychological adjustment: self-esteem,
depression
, sexual adjustment, and amount upset by
herpes
. Subjects were 152 people with
herpes
recruited from self-help groups and people from the community who volunteered to participate in the study. Results supported several hypotheses derived from previous research on coping with life stressors. Cognitive coping mechanisms, especially negative thoughts, along with wishful thinking and characterological self-blame, were significant predictors of poor psychological adjustment. In addition, the repeated use of disease management strategies was found to correlate with poor psychological adjustment. Further research in the area of coping with chronic illness is suggested.
...
PMID:Coping and adjustment to genital herpes. 654 39
Following transplant, circulating immunoglobulin levels fell moderately and remained depressed less than 2 months for IgG, and for variable and longer periods of time for IgM and IgA. Repeated quantitative determinations of antibodies against multiple antigens did not show any decrease in the pretransplant levels. Indeed some patients developed
herpes
and cytomegalovirus infections to which they responded by a sharp increase in antibody titers. In 2 cases, a primary immunization was demonstrated (against CMV and BK virus) with increasing levels of IgM and IgG antibodies. Lymphocyte counts in peripheral blood returned to 500 mm# between day 10 and 29 (median day 18) and to pretransplant values within 6 weeks. Non specific stimulation of lymphocytes by mitogens in the immediate post-transplant period showed a decreased response to PHA and Con A, whereas the responses to pokeweek mitogens and alloantigens were only slightly diminished. The degree of the responses was related to the dose of cryopreserved marrow infused. We conclude that:--although the minimum dose for autologous bone marrow transplantation in man is around 0,5 10(8) nucleated bone marrow cells/Kg, much higher doses should be used to ensure faster and better restoration of immune reactivity.--The similarity of the immunological dysfunction following autologous and allogeneous bone marrow transplantation suggest that, in the immediate post-transplant period, the role of GVHD in cellular immunity
depression
may be minimal.
...
PMID:[Studies of immunological status, following autologous bone marrow transplantation in man (author's transl)]. 700 23
In previous studies we found that the immunosuppression seen in mice bearing
Herpes
virus type 2-transformed (H238) fibrosarcoma was likely to be due to tumor-derived transforming growth factor-beta (TGF-beta). In vitro experiments showed that interleukin-2 (IL-2) and antibodies against TGF-beta could significantly counteract TGF-beta-induced
depression
in lymphocytes. The present study was performed to determine if the administration of polyclonal anti-TGF-beta antibody and recombinant IL-2, alone or in combination, could inhibit H238 tumor progression in vivo and to investigate possible mechanisms of action. The tumor cells were injected s.c. at 1 x 10(6) cells/mouse and treatments were given 1-10 days post-injection. In phase I, a total of 25,000 units of IL-2 (5,000 units/injection) and/or 900 ng of anti-TGF-beta (100 ng/injection) were administered i.p. per animal. Phase II was conducted similarly, except that each mouse received a total of 127,500 units of IL-2, either with or without the same amount of antibody. No treatment-related toxicity was noted. Tumor volumes were monitored for 16-18 days after tumor implantation. The H238 tumors in treated mice from both both phases grew as rapidly as, or significantly faster than, in untreated controls. Significant enhancement of tumor growth was found in the groups given IL-2 as a single agent, regardless of total dose. The combination of the higher IL-2 dose with anti-TGF-beta resulted in more rapid tumor progression than in animals given the antibody alone. Relative spleen weights, peripheral blood leukocyte counts, and the chemiluminescent oxidative burst of phagocytes were significantly elevated in all tumor-bearing mice, whereas T cell response to mitogenic stimulation was depressed. However, the oxidative burst capacity of spleen (but not blood) cells and natural killer cell cytotoxicity were markedly lower in the treated groups compared to nontreated tumor-bearing controls. In contrast, plasma levels of tumor necrosis factor-alpha and IL-2 were substantially higher in the group given both modalities (phase II) compared to the other treated groups. These findings show that anti-TGF-beta antibody, both with and without low-dose IL-2 regimens, can be safely administered in vivo. However, tumor growth was not delayed by the treatment protocols used. The induction of hyporesponsiveness in certain cell types may account, at least partly, for the enhancement seen in tumor progression.
...
PMID:Effects of anti-transforming growth factor-beta antibody and interleukin-2 in tumor-bearing mice. 780 55
We evaluated the effects of systemic infection by
Herpes
bovis virus 2 (HBV-2) on a murine experimental system. We provide evidence that such infection is lethal for the immunocompromised but not for the immunocompetent mouse in which a biphasic immune response is elicited. In particular, 1 day post-infection, we observed a rapid transient
depression
induced by the virus, as documented by a decrease in peripheral leukocyte counts, mitogenic spleen cell response and resistance to a secondary microbial challenge. Later, HBV-2 infection boosted cytokine secretion and enhanced antimicrobial and antitumoral activities by the splenic district. In conclusion, our experimental model discloses some immunological aspects underlying the complex host-virus interaction.
...
PMID:Systemic infection with Herpes bovis virus 2 evokes a biphasic immune response in the mouse. 786 83
The clinical and histological features of 49 lesions induced by human papillomavirus type 1 (HPV-1) were studied. The majority of cases showed the typical clinical features and location of such lesions. They were usually located on the ventral or lateral surfaces of the hands or feet, and were dome-shaped lesions with a central
depression
. However, HPV-1-induced lesions located on other body areas displayed different clinical features, such as those of common warts, a digitate wart, and a cutaneous horn. One lesion on a healing burn scar had a
herpes
-like appearance. As these 49 lesions were induced by the same type of HPV (HPV-1), differences in their clinical features are likely to have been due to host-related factors.
...
PMID:Varied clinical morphology of HPV-1-induced warts, depending on anatomical factors. 838 84
The American Social Health Association (ASHA) surveyed people with
herpes
about their experiences with the disease and its effect on their lives. A systematic sample of 5,000 was chosen from approximately 10,000 readers of the helper, ASHA's quarterly journal for people with
herpes
. Of the sample, 3,120 returned completed surveys, which addressed medical history, health-care experience, treatment, personal impact, and demographic information. Data analysis was descriptive, consisting of observed frequencies and cross-tabulations. Data illustrated that the psychosocial impact of
herpes
can be serious and long-lasting. Diagnosis is often associated with emotional upheaval, and dissatisfaction with diagnosing health-care providers was common. Over one-half of the respondents reported feelings of
depression
and fear of rejection in the last year. Sexual enjoyment and activity also were negatively affected by
herpes
. These results may be instructive to those delivering health services by providing insight into the significant impact of
herpes
on those infected.
...
PMID:Herpes revisited. Still a cause of concern. 850 63
This review addresses the importance of studies of human psychoneuroimmunology in understanding the role of psychological factors in physical illness. First, it provides psychologically and biologically plausible explanations for how psychological factors might influence immunity and immune system-mediated disease. Second, it covers substantial evidence that factors such as stress, negative affect, clinical depression, social support, and repression/denial can influence both cellular and humoral indicators of immune status and function. Third, at least in the case of the less serious infectious diseases (colds, influenza,
herpes
), it considers consistent and convincing evidence of links between stress and negative affect and disease onset and progression. Although still early in its development, research also suggests a role of psychological factors in autoimmune diseases. Evidence for effects of stress,
depression
, and repression/denial on onset and progression of AIDs and cancer is less consistent and inconclusive, possibly owing to methodological limitations inherent in studying these complex illnesses, or because psychological influences on immunity are not of the magnitude or type necessary to alter the body's response in these cases. What is missing in this literature, however, is strong evidence that the associations between psychological factors and disease that do exist are attributable to immune changes.
...
PMID:Health psychology: psychological factors and physical disease from the perspective of human psychoneuroimmunology. 862 35
Clinical electroencephalography is a relatively simple and inexpensive diagnostic tool with a high sensitivity for diffuse organic encephalopathy of various aetiologies but with a rather low specificity for the type of diagnosis. The highest sensitivity is shown in DAT and Parkinson dementia, and in these conditions the degree of EEG abnormality is correlated with the disease severity. Quantification of EEG makes these correlations more reliable and provides a method for monitoring therapeutic effects. Dementias with predominantly frontal pathology show much less EEG abnormality, and in these conditions the EEG is often normal despite obvious clinical dementia. Also, alcohol dementias often show normal EEG patterns. At an early stage of clinical evaluation, EEG may be useful in the discrimination of organic dementia from pseudodementia, because EEG is usually normal in
depression
, confusion, agitation and other psychiatric conditions. In pseudodementia due to intoxication with sedatives the EEG is usually dominated by diffuse beta activity. At the stage of differential diagnosis of an organic brain disorder, EEG cannot reliably discriminate between encephalopathies secondary to hydrocephalus, AIDS, cerebrovascular disease, B12 deficiency and primary degenerative diseases such as DAT. More specific EEG patterns are seen in acute cerebrovascular lesions, metabolic encephalopathies, i.e. of hepatic origin, Creutzfeldt-Jakob disease,
herpes
encephalitis, and nonconvulsive status epilepticus as possible causes of a rapidly deteriorating mental and neurological condition. Repeated EEG recordings over time would add significantly to the diagnostic information. New techniques such as topographical brain mapping, analysis of the EEG during REM sleep, coherence analysis of the EEG activity, and the combination of quantified EEG techniques with evoked potentials and event-related potentials will presumably add to the sensitivity as well as the specificity of the electrophysiological methods in the diagnosis of dementia.
...
PMID:Electroencephalography as a diagnostic tool in dementia. 906 24
<< Previous
1
2
3
4
5
Next >>