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Biomedical subjects

S Nielsen

Publications and source records attributed to S Nielsen.

At least 361 records · Page 20Linked to original sources
PubMed1983

Brainstem glioma: clinical manifestations of meningeal gliomatosis.

Brainstem gliomas of children are variably malignant tumors that rarely have been reported to produce subarachnoid dissemination. Nevertheless, during a two-year period, 5 of 15 such patients treated by us developed symptoms of leptomeningeal metastases. The diagnosis of an anaplastic astrocytoma with meningeal gliomatosis was confirmed postmortem in all 5. In 3 children, meningeal symptoms preceded other signs of posterior fossa recurrence. Symptoms of meningeal gliomatosis included local or radiating back pain (5 patients), segmental weakness (3), paresthesia (2), and incontinence (2). Myelography, performed in 4 patients, was the most useful diagnostic technique, disclosing multiple intradural filling defects or a high degree of block in 3 patients. Although the cerebrospinal fluid was abnormal in all 4 examined patients, in only 1 were malignant cells detected. Prolonged survival, which appears to predispose to dissemination of adult malignant gliomas, was not an apparent factor in our patients.

Adult↗
PubMed1983

Neurological complications of acquired immune deficiency syndrome: analysis of 50 patients.

Fifty patients with acquired immune deficiency syndrome had complications affecting the central or peripheral nervous systems or both. The patients were either male homosexuals, intravenous drug abusers, or recently arrived Haitian refugees. They ranged in age from 25 to 56. Central nervous system complications were of four kinds: (1) Infections included Toxoplasma gondii abscesses in 5 patients, progressive multifocal leukoencephalopathy in 2, cryptococcal meningitis in 2, Candida albicans in 1, and possible Mycobacterium avium intracellulare in 3. Eighteen patients suffered a subacute encephalitis possibly attributable to cytomegalovirus infection. (2) Tumors consisted of primary lymphoma of the brain in 3 patients and meningeal invasion by systemic lymphoma in 4. (3) Vascular complications included nonbacterial thrombotic endocarditis in 2 patients and cerebral hemorrhages in the setting of thrombocytopenia in 3. (4) Undiagnosed central nervous system problems were evidenced as focal brain lesions in 3 patients and self-limiting aseptic meningitis in 4. Peripheral neuropathy occurred in 8 patients.

Acquired Immunodeficiency Syndrome↗
PubMed1983

Syncope from head and neck cancer.

We have examined 17 patients suffering from recurrent syncope caused by carcinoma of the head and neck. The tumor originated in the mouth in seven, larynx in six, nasopharynx in three and parotid gland in one, and involved cervical lymph nodes at diagnosis in 12. Sixteen patients had previously had radical neck dissections and 12 had had radiation therapy. Recurrent carcinoma was present in 16. Spells resolved spontaneously in four, improved with treatment in 11 and continued in two. The syncope was spontaneous in 15 and induced only by suctioning or carotid sinus massage in two. Suctioning also produced attacks in four others, as did carotid sinus massage in five of ten tested. Acute severe unilateral head or neck pain preceded spontaneous syncope in 11. Sixteen patients had both profound bradycardia and hypotension during most spells, but ten had syncope with hypotension only, either spontaneously or following cardiac pacing or atropine to prevent bradycardia. Seizure activity accompanied syncope in eight. Anticholinergics improved 7/12, carbamazepine 2/5, carotid ligation 1/1 and intracranial sectioning of the glossopharyngeal nerve 1/1. Local radiation may have helped 4/10. Cardiac pacing was ineffective in 3/3 due to the development of pure vasodepressive syncope. Autopsy in 2/2 showed tumor involving the glossopharyngeal and vagus nerves. Syncope in these patients is under-recognized, frequently is due to vasodepression, and suggests recurrent carcinoma.

Aged↗
PubMed1979

A sensitive enzyme immunoassay for the quantitation of human IgM.

A highly sensitive and specific two-site solid-phase enzyme immunoassay for the quantitation of human immunoglobulin M (IgM) in biological fluids is presented. Detection limit is 20 micrograms/l (12 ng/tube). Routine working range is 30--1000 micrograms/l. Between-assay coefficient of variation is 10%. The assay allows quantitation of IgM in human cerebrospinal fluid.

Body Fluids↗
PubMed1976

Intracarotid BCNU (NSC-409962): a toxicity study in six rhesus monkeys.

Intracarotid artery (ica) BCNU was given at doses of 1-20 mg/kg/week for 4 weeks in six rhesus monkeys. Vascular, neurologic, and ophthalmic toxic effects were minor. The monkey receiving a dose of 15 mg/kg had transient left hemiparesis and slowing in her electroencephalogram which cleared 1 week after the third ica infusion of BCNU. At autopsy no vascular, neural, or ophthalmic lesions were found. At doses of 20 mg/kg for two injections, one monkey developed fatty metamorphosis of the liver and Alzheimer II glia in the brain, yet did not develop arteriolitis, corneal damage, or neurologic deficit. It is concluded that reasonable doses of BCNU (less than the systemic maximum tolerated dose) should be well tolerated by ica administration in man.

Animals↗
PubMed1975

Transformation of the rat uterine estrogen receptor after partial purification.

Warming crude ratuterine cytosol after the addition of [3H] estradiol accelerates the association of the 4-S estrogen-binding protein with a second macromolecule, resulting in the formation of the 5-S estrogen-binding protein. To determine whether the 5-S estrogen-binding protein consists of two similar or dissimilar subunits, uterine cytosol was subjected to a number of fractionation procedures that separate macromolecules by solubility, molecular gel sieving, sedimentation rate, ionic charge, and heat lability. Following each of these methods, the fraction containing the 4-S estrogen-binding protein was incubated at 28 degrees C; each of the these 4-S estrogen-binding protein-containing fractions retained its capacity to completely transform to the 5-S estrogen-binding protein. In samples subjected to partial purification procedures, it was necessary that the buffer contain 40 mM Tris, 60 mM Tris, 60 mM KC1, 1-10 MM dithiothreitol, and 1 M urea at pH 7.4, in order to accomplish the 4-S to 5-S estrogen-binding protein transformation at 25 degrees C. Formation of the 5-S estrogen-binding protein requires association of the 4-Estrogen-binding protein with a molecule identical to or very similar to itself.

Animals↗
PubMedDate not supplied

Afternoon cortisol levels before (spontaneous) and after suppression with dexamethasone or oxazepam in depressed patients.

In 35 hospitalized depressed patients afternoon plasma cortisol (15:00-15:20 h) was measured in 3 ways: spontaneous, 2 h after administration of 45 mg oxazepam, and 16 h after administration of 2 mg dexamethasone. Dexamethasone and oxazepam caused a marked suppression of cortisol secretion, the former being the most pronounced. A significant correlation between spontaneous and suppressed cortisol levels was found and a correlation between the suppressed cortisol levels was also demonstrated. Both spontaneous and suppressed cortisol values correlated with measures of type (Newcastle scales) and severity (Hamilton rating scale) of depression, and the highest correlations were obtained with cortisol values after dexamethasone suppression. Analysis of the items of the Hamilton rating scale for depression showed a high correlation with retardation (items 7 + 8) and somatic complaints (items 12 + 13). A high correlation with the items 8 + 9 + 10 + 12, as found in an earlier study, was also found in this study. On the basis of these findings it is concluded that hypersecretion of cortisol measured spontaneously or after suppression is not a true diagnostic measure (within a group of depressed patients), but reflects differences in the intensity of certain psychiatric symptoms constituting the depressive syndrome.

Adult↗
PubMedDate not supplied

Long-term bone loss in insulin-dependent diabetic patients with microvascular complications.

Insulin-dependent diabetic patients have an approximately 10% decreased bone mineral content (BMC) when they are studied a few years after clinical onset of diabetes. After that time, patients without diabetic microvascular complications have no, or only very little, further bone loss. The aim of the present study was to investigate if any substantial long-term bone loss occurs in diabetic patients with microvascular complications. We studied 19 insulin-dependent diabetic patients with neither physiologic nor pathologic conditions known to interfere with bone metabolism, other than diabetes. BMC was determined twice, with an interval of 11 years. At initial examination, no patient had diabetic microangiopathy, but at final examination 7 patients had developed diabetic microvascular complications while 12 patients had not. As compared with gender- and age-matched controls, both subgroups had significantly decreased BMC at the initial examination. During the study period, the patients with complications showed further bone loss, whereas the subgroup without complications had unchanged decreased BMC. At final examination, BMC was significantly lower in patients with microvascular complications than in patients without them. The biochemistry of bone metabolism showed a significantly increased fasting urinary excretion of calcium and hydroxyproline in patients with complications, but not in the group without complications, and there was a negative correlation between plasma BGP (osteocalcin) and hemoglobin A1C for all patients. These findings indicate that, in addition to a decreased BMC (before or shortly after clinical onset of diabetes), patients who develop microvascular complications also develop ongoing bone loss. This loss may be caused by an increased bone resorption, but decreased bone formation during periods of poor diabetic control may be involved as well.

Adult↗