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Biomedical subjects

C Orellana

Publications and source records attributed to C Orellana.

28 records · Page 2Linked to original sources
PubMed1996

Earliest memories and recall by modality usually involve recollections of different memories: memories are not amodal.

66 students recalled a first memory and indicated whether sensory impressions from each sensory modality were a part of this memory and, if so, how clear and important these impressions were. After a distraction, they also recalled in each sense modality the very first memory they could. Only visual impressions were always a part of first memories. The clarity and importance of sensory attributes were evaluated similarly. Recall by modality led to memories of equivalent clarity, and these were usually memories other than the one recalled as the earliest memory or recalled using other modalities. Memories are more modality-specific than assumed before in theory or practice.

Adolescent↗
PubMed1996

Only visual impressions are almost always present in long-term memories, and reported completeness, accuracy, and verbalizability of recollections increase with age.

In two studies, students answered questions about their earliest memories from childhood and either elementary school and high school or college and yesterday. Visual sensory impressions were present in all childhood and almost all later memories. Sound aspects were more frequent in memories from high school and college than in those from childhood. Earliest memories from yesterday almost always included internal sensations. Recollections were rated as more accurate, complete, and verbalizable as events occurred later in life. Memories from childhood, elementary, and high school were thought about, found useful, or shared equally frequently. Yesterday's events were less likely shared, but, if shared, enhanced social relationships.

Adolescent↗
PubMed1996

Reduced serum creatine kinase activity in inflammatory rheumatic diseases.

OBJECTIVE: To determine if serum CK activity is reduced in inflammatory rheumatic diseases and to evaluate whether this phenomenon is linked to disease activity or steroid therapy. METHODS: Serum CK activity was measured in patients with systemic lupus erythematosus (SLE, n = 52), rheumatoid arthritis (RA, n = 80), ankylosing spondylitis (AS, n = 82), spondyloarthropathies other than AS (SpA, n = 22), and a miscellaneous group (MI, n = 27), and in 103 control patients with noninflammatory arthropathies (NIA). Laboratory variables of inflammatory activity such as ESR, CRP, platelet count, and hemoglobin (and anti-DNA antibodies and complement levels in SLE) were measured at the same time. Daily dose of steroids was also evaluated. RESULTS: Serum CK activity was significantly reduced in SLE (mean +/- SD: 49 +/- 41 IU/l), RA (68 +/- 41 IU/l), SpA (88 +/- 53 IU/l), and MI (75 +/- 32 IU/l) compared to controls (111 +/- 38 IU/l) (p = 0.002 for SpA and p < 0.001 for the other groups). No differences in CK values were observed between AS and controls, although AS patients with peripheral arthritis had lower serum CK activity than those without (80 +/- 32 vs 121 +/- 62 IU/l, respectively, p < 0.05. ESR, CRP, and platelets correlated inversely with CK values in RA, AS, and MI. In the SpA group only ESR correlated inversely with CK. In SLE, a positive correlation was found between CK values and CH50 and a negative one with anti-DNA levels. Patients taking steroids had significantly lower CK activity than those without corticotherapy. However, multivariate analysis showed that only inflammatory activity and no steroids had an effect in reducing CK activity. CONCLUSION: Serum CK activity is significantly reduced in several inflammatory rheumatic diseases. Inflammatory activity seems to play the major role in this phenomenon.

Adult↗
PubMed1995

When does amyloidosis complicate systemic lupus erythematosus?

Secondary amyloidosis is a well recognised complication of rheumatic diseases, but the association with systemic lupus erythematosus is very unusual. We report the case of a patient with systemic lupus erythematosus who developed proteinuria due to renal amyloidosis. We also review the cases previously reported and the hypothesis on the pathogenic mechanisms.

Adult↗
PubMed1995

Monomelic hypertrophic osteoarthropathy secondary to aortic prosthesis infection.

We describe a case of hypertrophic osteoarthropathy (HOA), exclusively located in the left lower leg and secondary to vascular prosthesis infection. Four years before, the patient underwent aortofemoral bifurcation grafting because of a ruptured aortic aneurysm. The investigations revealed prosthesis infection by Pseudomona aeruginosa and Bacteroides thetaiotamicron. The onset of HOA in a patient with a vascular prosthesis can help to achieve an early diagnosis of graft infection. The literature on this uncommon association is reviewed.

Aorta↗
PubMed1994

Life events in the year preceding the onset of narcolepsy.

A multifactorial etiology for narcolepsy has been postulated, stressing the importance of environmental factors in the clinical onset of the condition. Our study evaluated the occurrence of stressful life events in the year preceding the onset of narcolepsy. Fifty narcoleptic and 50 control subjects completed a life event questionnaire (the Schedule of Recent Experiences). The proportion of narcoleptic subjects reporting the presence of life events in the year preceding the onset of narcolepsy was significantly greater than the proportion of control subjects reporting life events in the corresponding year. Moreover the weight of life events was increased in narcoleptic subjects in comparison with controls. In conclusion life events seem to be increased in narcoleptic subjects in the year preceding the onset of their condition. However a number of other factors could not be taken into consideration, which limits the full significance of these data.

Adolescent↗
PubMed1991

Effects of selective activation or blockade of the histamine H3 receptor on sleep and wakefulness.

The effects of the histamine H3 receptor agonist, (R)-alpha-methylhistamine were compared with those of the histamine H3 antagonist, thioperamide, in rats implanted with electrodes for chronic sleep recordings. (R)-alpha-Methylhistamine (1.0-4.0 micrograms) injected bilaterally into the premammillary area where histamine immunoreactive neurons have been detected increased slow wave sleep, whereas wakefulness and REM sleep were decreased. No significant effects were observed when (R)-alpha-methylhistamine (1.0-8.0 mg/kg) was administered i.p. Thioperamide (1.0-4.0 mg/kg i.p.) increased wakefulness and decreased slow wave sleep and REM sleep. Pretreatment with thioperamide (4.0 mg/kg) prevented the effects of (R)-alpha-methylhistamine (2.0 micrograms) on slow wave sleep and wakefulness. Our results further support an active role for histamine in the control of the waking state.

Animals↗
PubMed1990

Sleep variables are unaltered by zolantidine in rats: are histamine H2-receptors not involved in sleep regulation?

The effects of the H1-receptor antagonist diphenhydramine and the brain-penetrating H2-receptor antagonist zolantidine were studied in rats implanted for chronic sleep recordings. Diphenhydramine (1.0-4.0 mg/kg) significantly increased slow wave sleep and decreased wakefulness. Zolantidine (0.25-8.0 mg/kg) had no significant effects on any of the sleep parameters examined. One possibility is that zolantidine did not enter the brain in sufficient concentration to produce significant changes on sleep and wakefulness. Another possibility is that blockade of H2-receptor involved parts of the brain other than those implicated in the sleep-wake cycle. The feasibility remains that H2-receptors are not involved in sleep regulation. The absence of selective, brain-penetrating H2-receptor agonists precludes a more detailed analysis of the role of this subtype of receptor in the control of sleep and wakefulness.

Animals↗
PubMed1987

Inhibition of adrenomedullary catecholamine release by propranolol isomers and clonidine involving mechanisms unrelated to adrenoceptors.

1 Transmural electrical stimulation (10 Hz, 40 V, 1 ms for 60s) increased total catecholamine secretion from perfused cat adrenal glands; this response was enhanced by neostigmine and inhibited by mecamylamine, suggesting that release of acetylcholine from splanchnic nerve terminals was stimulating nicotinic receptors and enhancing catecholamine secretion. 2 Isoprenaline, (-)-propranolol and (+)-propranolol (10(-7)-10(-5)M) inhibited the electrically-evoked secretory response by 40-70%; similar reductions were obtained with clonidine and yohimbine. Neither, (+)-propranolol nor (-)-propranolol inhibited K-evoked secretion from cat adrenals; in contrast, nimodipine potently inhibited it (IC50 = 24 nM). 3 Either, racemic propranolol or the (+)- or (-)-isomers (1-10 microM) equally inhibited [3H]-noradrenaline release evoked by nicotine or acetylcholine from cultured bovine adrenal chromaffin cells; clonidine (10 microM) inhibited secretion by 50% and yohimbine or isoprenaline did not affect it. 4 The results indicate that adrenomedullary catecholamine release evoked by splanchnic nerve stimulation is not modulated by alpha- or beta-adrenoceptors and suggest that propranolol may inhibit secretion by blocking ion fluxes through the acetylcholine receptor ionophore. Clonidine may inhibit secretion by this same mechanism, and/or by interfering with some intracellular event in the secretory mechanism.

Adrenal Medulla↗