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Biomedical subjects

M Weise

Publications and source records attributed to M Weise.

At least 19 recordsLinked to original sources
PubMed2002

Acute intramural haematoma of the coeliac artery.

The report describes a previously healthy 24-year-old women presenting with acute abdominal pain following a hyperextension manoeuvre. The key finding of a continuous bruit with systolic and diastolic components in the epigastric region subsequently led to the diagnosis of an intramural haematoma of the coeliac artery, that caused a subtotal occlusion of the artery. The diagnosis was achieved by both colour-coded duplex sonography and magnetic resonance angiography. The case shows that a conservative management rather than operative reconstruction is justified in an oligo-symptomatic situation with no signs of end-organ damage as in this patient.

Acute Disease↗
PubMed2002

Pseudo-meigs syndrome: uterine leiomyoma with bladder attachment associated with ascites and hydrothorax - a rare case of a rare syndrome.

INTRODUCTION: Pseudo-Meigs syndrome is a rare syndrome with pelvic tumors (not ovarian fibromas), which is combined with ascites and hydrothorax. Up to now 23 cases of pseudo-Meigs syndrome associated with uterine leiomyomas are described. We present a further case of a young woman with pseudo-Meigs syndrome combined with bladder attachment and elevated CA-125. CASE REPORT: A 27- year-old woman complained about increasing abdominal volume for about 2 months. Clinical results showed a normal sized uterus with a pedunculated leiomyoma, ascites, and a small pleural effusion. CA-125 levels were approximately more than 50 times higher than normal range. An explorative laparotomy revealed a leiomyoma and ascites. The myoma was attached to the posterior wall of the bladder; the rest of the uterus and both adnexae were normal. An organ-preserving operation was performed. Three months afterwards the patient presented normal clinical and sonographical findings and normal CA-125 serum levels. DISCUSSION: Uterine leiomyoma is only rarely associated with ascites and hydrothorax. Our case is the 24th in literature. Like other authors we could show elevated CA-125 serum levels. Cases of pseudo-Meigs syndrome with penduculated myomas and tight adhesions of neighbouring structures have been described frequently. In our case the bladder was tightly attached, and the vascularisation seemed to come from the uterus and the bladder. This atypical double supply might be in etiological context with the ascites. Pseudo- Meigs syndrome should be considered as a rare differential diagnosis for ascites and pleural effusions.

Adult↗
PubMed2001

Effects of estrogen on growth plate senescence and epiphyseal fusion.

Estrogen is critical for epiphyseal fusion in both young men and women. In this study, we explored the cellular mechanisms by which estrogen causes this phenomenon. Juvenile ovariectomized female rabbits received either 70 microg/kg estradiol cypionate or vehicle i.m. once a week. Growth plates from the proximal tibia, distal tibia, and distal femur were analyzed after 2, 4, 6, or 8 weeks of treatment. In vehicle-treated animals, there was a gradual senescent decline in tibial growth rate, rate of chondrocyte proliferation, growth plate height, number of proliferative chondrocytes, number of hypertrophic chondrocytes, size of terminal hypertrophic chondrocytes, and column density. Estrogen treatment accelerated the senescent decline in all of these parameters. In senescent growth plates, epiphyseal fusion was observed to be an abrupt event in which all remaining chondrocytes were rapidly replaced by bone elements. Fusion occurred when the rate of chondrocyte proliferation approached zero. Estrogen caused this proliferative exhaustion and fusion to occur earlier. Our data suggest that (i) epiphyseal fusion is triggered when the proliferative potential of growth plate chondrocytes is exhausted; and (ii) estrogen does not induce growth plate ossification directly; instead, estrogen accelerates the programmed senescence of the growth plate, thus causing earlier proliferative exhaustion and consequently earlier fusion.

Animals↗
PubMed2001

Catch-up growth is associated with delayed senescence of the growth plate in rabbits.

In mammals, release from growth-inhibiting conditions results in catch-up growth. To explain this phenomenon, we proposed the following model: 1) The normal senescent decline in growth plate function depends not on age per se, but on the cumulative number of replications that growth plate chondrocytes have undergone. 2) Conditions that suppress growth plate chondrocyte proliferation therefore slow senescence. 3) After transient growth inhibition, growth plates are thus less senescent and hence show a greater growth rate than expected for age, resulting in catch-up growth. To test this model, we administered dexamethasone to growing rabbits to suppress linear growth. After stopping dexamethasone, catch-up growth occurred. In distal femoral growth plates of untreated controls, we observed a senescent decline in the growth rate and in the heights of the proliferative zone, hypertrophic zone, and total growth plate. During the period of catch-up growth, in the animals previously treated with dexamethasone, the senescent decline in all these variables was delayed. Prior treatment with dexamethasone also delayed epiphyseal fusion. These findings support our model that linear catch-up growth is caused, at least in part, by a delay in growth plate senescence.

Animals↗
PubMed2000

Adrenomedullary dysplasia and hypofunction in patients with classic 21-hydroxylase deficiency.

BACKGROUND: Glucocorticoids are essential for the normal development and functioning of the adrenal medulla. Whether adrenomedullary structure and function are normal in patients with congenital adrenal hyperplasia is not known. METHODS: We measured plasma and urinary catecholamines and plasma metanephrines in 38 children with congenital adrenal hyperplasia due to 21-hydroxylase deficiency (25 children with the salt-wasting form and 13 with the simple virilizing form), 39 age-matched normal subjects, and 20 patients who had undergone bilateral adrenalectomy. Adrenal specimens obtained from three other patients with 21-hydroxylase deficiency who had undergone bilateral adrenalectomy and specimens obtained at autopsy from eight other patients were examined histologically. RESULTS: Plasma epinephrine and metanephrine concentrations and urinary epinephrine excretion were 40 to 80 percent lower in the patients with congenital adrenal hyperplasia than in the normal subjects (P<0.05), and the values were lowest in the patients with the most severe deficits in cortisol production. Urinary epinephrine excretion and plasma epinephrine concentrations were at or below the limit of detection of the assay in 8 (21 percent) of the patients with congenital adrenal hyperplasia and in 19 (95 percent) of the patients who had undergone adrenalectomy. In the group of patients with congenital adrenal hyperplasia, plasma epinephrine and metanephrine concentrations and urinary epinephrine excretion were approximately 50 percent lower in those who had been hospitalized for adrenal crises than in those who had not. In three patients with congenital adrenal hyperplasia who had undergone bilateral adrenalectomy, the formation of the adrenal medulla was incomplete, and electron-microscopical studies revealed a depletion of secretory vesicles in chromaffin cells. CONCLUSIONS: Congenital adrenal hyperplasia compromises both the development and the functioning of the adrenomedullary system.

Adolescent↗
PubMed1999

Pneumatic external counterpulsation: a new noninvasive method to improve organ perfusion.

Pneumatic external counterpulsation, which is operated by applying electrocardiographic-triggered diastolic pressure via air-filled cuffs to the vascular limbs of lower limbs, is a relatively new therapeutic option for patients with angina pectoris and cerebrovascular diseases like transient ischemic attacks or sudden deafness. In this study, an augmentation in flow volume in the carotid, renal, and hepatic arteries from 20% to 25% and in the coronary arteries from 20% to 40%, as well as an increase in stroke volume by 12% was demonstrated; this shows the therapeutic results in patients with diseases caused by disturbed organ perfusion.

Adult↗
PubMed1999

[Transesophageal imaging of a coronary fistula in simultaneous endocarditis lenta].

A 61 year old diabetic patient with bacterial endocarditis probably caused by a congenital coronary fistula is presented. The fistula was already detected by transthoracic echocardiography. Transesophageal color-Doppler echocardiography identified the precise localization and course of the fistula. Additionally, in some parts of the fistula echogenic material could be seen that decreased in size after antibiotic treatment. Therefore, it was considered as corresponding to bacterial vegetations. Coronary angiography disclosed an ectopic aneurysmatic and elongated circumflex coronary artery. Thus, even in rare conditions such as coronary fistulas transesophageal echocardiography may be helpful to allow detection of morphological substrate of associated infective endocarditis.

Coronary Thrombosis↗
PubMed1999

Leptin secretion in Cushing's syndrome: preservation of diurnal rhythm and absent response to corticotropin-releasing hormone.

The normal inverse relationship between leptin and cortisol is lost in chronic hypercortisolism. We studied this apparent dysregulation in patients with Cushing's syndrome to investigate 1) the effect of chronic hypercortisolemia on the circadian rhythm of leptin secretion, 2) the response of leptin after administration of CRH, and 3) the short term effect of curative surgery on leptin. The preoperative morning leptin concentration was 54.2 +/- 8.1 ng/mL, and the nighttime value was 68.6 +/- 9.8 ng/mL, reflecting a mean rise of 32.8 +/- 7.6%, similar to the nocturnal increase observed in normal subjects. By contrast, cortisol's diurnal variation (21.8 +/- 1.7 vs. 16.9 +/- 1.1 mg/dL) was blunted. In women, but not men, body mass index correlated with leptin (P = 0.001). Preoperative ACTH and cortisol (both P < 0.0001), but not leptin levels increased after CRH. Ten days after surgery, basal cortisol values were subnormal (1.1 +/- 0.6 mg/dL), but leptin levels remained unchanged and did not increase after CRH. Body mass index and insulin also remained unchanged. Insulin, but not age, urinary free cortisol, or plasma cortisol correlated with leptin (P < 0.05). In summary, patients with Cushing's syndrome have moderately elevated leptin levels that maintain an intact circadian rhythm but do not respond to acute or subacute alterations of cortisol.

Adenoma↗
PubMed1997

Direct and indirect memory measures of temporal order: younger versus older adults.

The memory changes associated with age are attributed to the deterioration of the frontal lobes, as well as to the middle temporal structures. Therefore, in addition to a decline in memory for facts and events, as found impaired in amnesics, a memory decline associated with age is predicted for tasks typically found impaired in frontal lobe patients (i.e., temporal order judgment). There are conflicting findings concerning whether indirect measures of memory for facts and events are associated with age. However, there are no studies that address this issue with regard to temporal order judgment. Thirty younger and thirty older adults were tested on a list of words which was repeated five times in fixed or varying order. The number of words recalled, as well as their temporal judgments, were the direct measure of memory. The effect of consistency of order of presentation on the number of words recalled was the indirect measure of memory for temporal order. Results suggest that direct, but not the indirect measures of memory were related to age.

Adult↗
PubMed1993

Protection from reperfusion-induced arrhythmias by polyethylene glycol 600.

The effects of polyethylene glycol (PEG) 600 on cardiovascular parameters and reperfusion-induced arrhythmias were investigated using a 5-min period of ligation of the left anterior descending coronary artery followed by reperfusion in an anaesthetized open-chest rat model. PEG 600 was effective in reducing reperfusion arrhythmias, such as ventricular fibrillation and ventricular tachycardia. Mortality was decreased from 29.4% (5/17) in the saline-control to 0% (0/14) in the PEG-treated group (P < 0.05). Biochemical investigations during the ischaemia/reperfusion period revealed that PEG infusion resulted in a reduction of cardiac lactate as well as a striking maintenance of the glutathione content of the heart.

Animals↗
PubMed1993

Glucose metabolism in Ullrich Turner syndrome: long-term effects of therapy with human growth hormone. German Lilly UTS Study Group.

The effects of GH therapy on glucose metabolism in 72 Turner patients treated with human GH (HGH) 2, 3 or 4 IU/m2/day for 2 years are reported. OGTTs were performed at 0, 3, 12 and 24 months. The overall frequency of glucose intolerance was 9.7% before therapy and did not change under HGH. No change in HbA1c and fasting glucose values occurred. Integrated blood sugar values in the OGTT (area under the curre) did not change with 2 and 3 IU but were significantly elevated over control after 2 years with 4 IU. Insulin secretion was not significantly affected over time with 2 IU, whereas 3 and 4 IU produced significant increases which persisted after 2 years. Results indicate that glucose homeostasis is maintained under GH therapy at the expense of a compensatory increase in insulin secretion which persists at higher GH dosages.

Adolescent↗
PubMed1993

Dose-dependent effect of growth hormone therapy on glucose metabolism in subjects with Turner syndrome. The German Lilly Ullrich-Turner Syndrome Study Group.

Recombinant human growth hormone (GH) is effective in promoting growth velocity in subjects with Turner syndrome. As higher doses are used for this indication than for substitution therapy in GH deficiency, the long-term effects of GH therapy on carbohydrate metabolism represent a safety issue; this is particularly important in Turner syndrome, in which there is an increased prevalence of impaired glucose tolerance. So far, GH therapy has been given to patients with Turner syndrome for up to 7 years without any significant changes having been reported in glycosylated haemoglobin (HbA1c) values, unstimulated and stimulated oral glucose tolerance test (OGTT) blood glucose and serum insulin concentrations. These findings may, however, be influenced by other variables, such as study design, number of subjects or standardization methods applied. Results of an ongoing trial in the FRG, from which 2 years' data on glucose metabolism (as assessed by serial OGTTs) of 72 patients with Turner syndrome are available, indicate that glucose homoeostasis is maintained at the expense of an increase in insulin secretion, which is time- and dose-dependent. Although these changes may be fully reversible on withdrawal of GH. therapy, accurate control of glucose metabolism both during and after GH. treatment is advocated.

Blood Glucose↗
PubMed1992

Effect of isoniazid or phenobarbital pretreatment on the metabolism of dihalomethanes to carbon monoxide.

An oral dose of 6.2 mmoles of diachloromethane (DCM), bromochloromethane (BCM) or dibromomethane (DBM) per kg body mass yielded a maximum carboxyhemoglobin (COHb) level of about 9% (at 6 hr), 11% (at 8 hr) and 22% (at 12 hr), respectively. Pretreatment of rats with isoniazid, 4 x 0.36 mmol/kg i.p., produced significant enhancements of the COHb formation; the values were 18.0 +/- 0.8% COHb after DCM, 24.1 +/- 0.8% COHb after BCM, and 39.0 +/- 1.3% COHb after DBM. Prior administration of phenobarbital, 4 x 0.31 mmol/kg i.p., caused no appreciable alterations in the COHb levels after DCM and slight but significant increases after BCM as well as after DBM. The data indicate that the oxidative metabolism of dihalomethanes to carbon monoxide is mainly catalyzed by cytochrome P-450 IIE1 and that the DCM-evoked COHb formation seems to be a method of testing whether a chemical is an inducer of this form of cytochrome P-450 in vivo.

Animals↗