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T Lohmann

Publications and source records attributed to T Lohmann.

46 records · Page 3Linked to original sources
PubMed1996

T cell clones to epitopes of glutamic acid decarboxylase 65 raised from normal subjects and patients with insulin-dependent diabetes.

Insulin-dependent diabetes (IDDM) is probably mediated by T lymphocytes recognizing critical beta cell autoantigens. Glutamic acid decarboxylase (GAD) 65 is a major antigen in IDDM. T cells in both IDDM patients and controls respond to GAD 65 and certain epitopes of this molecule. To clarify the immune response to GAD 65 we established T cell clones specifically recognizing epitopes of GAD 65. We obtained T cells clones to GAD 65 peptides 161-175 (from a healthy individual), and 505-519 and 521-535 (from two IDDM patients). On extensive screening T cells responsive to peptide 161-175 were found only in controls, while T cells responsive to peptide 521-535 were found only in IDDM patients; T cells from both IDDM patients and controls responded to peptide 505-519. We could exclude simple genetic shaping of these T cell responses since the responses differed between genetically identical twins discordant for IDDM. Reactivity of T cell clones from the control to peptide 161-175 was restricted by HLA DR1 but promiscuous for HLA DR4 as DR4+ EBV transformed B cells and DR4+ mouse L-transfectants could present the peptide. As DR4+ antigen presenting cells of diabetics could present peptide 161-175 to some clones, the lack of response to this epitope in diabetic patients cannot be due to inadequate antigen presentation but is probably due to deletion of these cells either centrally or peripherally. Reactivity of clones to peptide 505-519 was either HLA DR1 or DQ1 restricted. In conclusion, T cell clones to specific epitopes of GAD 65 provide a model to clarify those differences in the immune response to this autoantigen between controls and IDDM patients.

Antibody Formation↗
PubMed1996

[Successful electroconvulsive therapy of Cotard syndrome with bitemporal hypoperfusion].

A case study is presented to illustrate a rare condition described by Cotard as "délire de négation". The central symptom is a nihilistic delusion with denial of one's own existence of oneself and that of the external world. In the present case, the syndrome became manifest as an escalation of a recurrent depressive disorder late in life. After initial resistance to therapy, the syndrome was successfully treated with electroconvulsive therapy. For the first time, we report the regional cerebral blood flow measured by 99mTc-HMPAO-SPECT before and after therapy. Before treatment, significant bitemporal hypoperfusion relative to the cerebellum was found, which was no longer demonstrable on remission.

Aged↗
PubMed1995

A unique case of tardive dystonia induced by short-term therapy with perazin.

Perazin is a piperazine derivative of phenothiazine with higher affinity for the D2 than the D1 receptor. We observed a 43-year-old woman who developed blepharospasm and oral hyperkinesia as a tardive dystonic syndrome after short-term treatment with perazin. She had never taken any other neuroleptic medication and all known forms of secondary dystonia were ruled out. We were unable to find any previous reports of perazin-induced tardive dystonia.

Adult↗
PubMed1994

Immunodominant epitopes of glutamic acid decarboxylase 65 and 67 in insulin-dependent diabetes mellitus.

To find the dominant epitopes of a major autoantigen in insulin-dependent diabetes mellitus (IDDM), glutamic acid decarboxylase (GAD), we studied the reactivity of peripheral blood T lymphocytes with peptides covering both major isoforms. A significant response to GAD 65 or GAD 67 peptides was detected in 13 of 15 IDDM patients and in 9 of 10 normal controls. Controls most frequently recognised the central region of GAD 65 (residues 161-243). IDDM patients preferentially recognised residues 473-555 (p < 0.03). T-cell responses to GAD 67 peptides were similar in IDDM patients and controls. T lymphocytes from IDDM patients recognise a distinct dominant epitope of GAD, which may be an important target for the disease process.

Adolescent↗
PubMed1993

[Effect of myelography on the curve of the auditory evoked early brain stem potentials].

In 50 patients auditory threshold and brain stem evoked potential studies were carried out before and after myelography. Due to the analysis of amplitudes and latencies of auditory brain stem measurements, significant functional disorders of the hearing organ and the auditory pathway could be demonstrated. In most of the patients these functional disorders were found to be subclinical, whereas 12 patients showed alterations extending from a subjectively slight hearing loss to an audiometrically objectified acute hearing loss depending on its intensity in each case. The reasons of these functional disorders could not be clarified. An open cochlear aqueduct through which perilymph enters the subarachnoidal space leading to a secondary endolymphatic hydrops can be considered as the cause in cases where manifest symptoms develop. The changes in brain stem audiometry can be additionally explained by changes in osmolality of the inner ear fluids which may lead to the development of an endolymphatic hydrops.

Auditory Pathways↗
PubMed1993

Low calorie unrestricted protein diet attenuates renal injury in hypertensive rats.

In the present investigation we researched the effects of low calorie diet without protein restriction on the renal function and glomerular injury of uninephrectomized spontaneously hypertensive rats. We compared the findings with those that occurred in two different groups of uninephrectomized spontaneously hypertensive rats: one treated with oral hydralazine (10 mg/kg per day) and a second fed regular food. The low calorie diet and hydralazine treatment significantly reduced intra-arterial blood pressure in each group (p < 0.05 and p < 0.001, respectively). The control group showed at the end of the experiment a slight but not significantly different increase in the intra-arterial blood pressure. Low calorie diet was more effective in protecting the kidney function. Creatinine clearance after treatment was significantly higher in uninephrectomized spontaneously hypertensive rats on a low calorie diet than in either the hydralazine-treated or control groups (p < 0.01). The 24-hour urinary protein excretion in the low calorie diet group was significantly lower than in the control group (p < 0.05) and lower but not statistically different from the hydralazine-treated group. The mean glomerular injury index of the remaining kidney in the low calorie diet group was lower than in either the hydralazine-treated or control groups (p < 0.05), and the mean mesangial expansion index in the low calorie diet group was significantly lower than in the control group (p < 0.05). The favorable effect of low calorie diet on renal function was independent of protein restriction or sodium and potassium content.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Adiponectin in patients with obstructive sleep apnea syndrome: course and physiological relevance.

BACKGROUND: Adiponectin is an adipocyte-derived hormone with anti-inflammatory and insulin-sensitizing properties. Insulin resistance is a typical feature of the obstructive sleep apnea syndrome (OSAS). OBJECTIVES: Since nasal continuous positive airway pressure (nCPAP) treatment improves insulin sensitivity in patients with OSAS, we investigated serum adiponectin levels before and during nCPAP treatment to clarify possible interactions between the adiponectin levels and insulin sensitivity in patients with OSAS. METHODS: Thirty nondiabetic, obese patients with OSAS (mean age 56.4 +/- 11.1 years; apnoea-hypopnoea index (AHI) 46.03 +/- 19.57) underwent CPAP treatment. Adiponectin levels and the levels of proinflammatory cytokines and proteins reflecting platelet activation [regulated on activation normally T cell expressed and secreted (RANTES) and soluble P-selectin (sCD62p)], as well as the insulin sensitivity index were measured before, and after 2 days and 3 months of CPAP treatment. RESULTS: Insulin sensitivity increased significantly under nCPAP treatment, whereas adiponectin levels decreased after 2 days of nCPAP treatment, but returned to baseline levels after 3 months of nCPAP treatment. The increase in insulin sensitivity was more pronounced in patients with the highest adiponectin levels at baseline (p = 0.021) after adjustment for body fat (p = 0.003). During treatment, changes in adiponectin levels were highly predictable by the insulin sensitivity index. CONCLUSIONS: We found a significant relation between adiponectin and the insulin sensitivity index in overweight patients with OSAS. The lack of a long-lasting change in adiponectin may be explained by the overwhelming influence of the body mass index on adiponectin secretion, which was unchanged during nCPAP treatment.

Aged↗
PubMedDate not supplied

The mercy of adrenocortical tumor cells on lymphocytes.

Immunologic escape includes the loss of Fas-receptor and the gain of Fas-ligand expression. Normal adrenal glands express the Fas-receptor and MHC class II molecules in inner cortical zones. A distinctive feature of adrenocortical tumors is the loss of MHC class II expression. Here we demonstrate loss of Fas and gain of Fas-ligand expression in the adrenocortical carcinoma cell line NCI-H295 by immunohistochemistry and RT-PCR. In a co-culture system of tumor cells and HLA-matched leukocytes, CD 8-positive or CD 4-positive lymphocytes, we examined the immunologic escape and the ability to induce apoptosis in the immune cells. The direct co-culture with either leukocytes, CD 8-positive or CD 4-positive lymphocytes reduced spontaneous apoptosis in immune cells from 49.9% to 13.0%, 8.6% and 15.3%, respectively, as determined by FACS analysis of Annexin V binding and LDH release in the medium. In co-culture, cortisol secretion increased up to 200%. Cellular communication does not induce apoptosis in immune cells, but promotes their survival. This may be due to partial HLA class I mismatches contributing to immunologic activity. The viability of the tumor cells was not affected, and these cells were stimulated to secrete cortisol. In summary, immune escape of adrenocortical carcinomas may occur because of altered Fas/Fas-L system expression and loss of MHC class H expression.

Adrenal Cortex Neoplasms↗