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Biomedical subjects

S Mukerji

Publications and source records attributed to S Mukerji.

At least 19 recordsLinked to original sources

Plastic surgery and the teenage patient.

Over the past year, the media have reported an increase in the number of teenagers undergoing plastic surgery, and with a tone of faint alarm have suggested that this merits some cultural self-scrutiny. This paper presents the statistics on the number and types of plastic surgery operations done in teenagers over the last eight years and discusses these in the context of cultural influences and societal concepts of beauty. The reason to have plastic surgery is psychological and involves body image, which is defined as the subjective perception of the body as it is seen through the mind's eye. To explain why changing the external appearance affects personality and behavior, the complex psychological reactions that occur after an operation that alters the size or shape of a body part are reviewed. Body image development occurs in stages, and puberty stands out as a particularly sensitive time as the teenager undergoes major changes in his or her physical appearance and does this at a time of heightened vulnerability to the opinion of others. Plastic surgery to correct a truly unattractive feature is enormously successful and remarkably free of conflict in this population. Teenagers undergo a rapid reorganization of their self-image after plastic surgery with subsequent positive changes in behavior and interpersonal interactions. The key to achieving success with plastic surgery is patient selection. The core value of the surgery lies not in the objective beauty of the visible result, but in the patient's opinion of and response to the change. Good patient management includes selecting candidates with clear and realistic expectations who are free of psychopathology. There must be true informed consent and attention to psychological issues must continue into the postoperative period. It is the responsibility of the patient's physician and plastic surgeon to recognize a need for psychiatric evaluation and to help the patient get this as needed. The eight operations most commonly done in the teenage population are rhinoplasty, ear surgery, reduction mammoplasty, surgery for asymmetric breasts, excision of gynecomastia, augmentation mammoplasty, chin augmentation, and suction assisted lipoplasty. Each of these is reviewed with regard to techniques, expectations, risks, and logistics. Guidelines for timing the referral of teenage patients for plastic surgery evaluation are given.

Adolescent↗

Psychological impact of the Antarctic winter on Indian expeditioners.

The authors studied the psychological variables of 25 men who participated in the winter-over team of an Indian expedition to Antarctica for possible associations with seasonality and isolation. It was found that increased cigarette smoking was associated with the stress of the beginning of isolation (March), sleep difficulty was associated with midwinter (June), rapport was at a minimum at the point of maximum isolation in temporal terms (September), and decreased satisfaction with work and life situations was associated with continued isolation (December, January). The study suggested that variables postulated to affect performance undergo changes during the course of wintering over in Antarctica.

Adaptation, Psychological↗

Simulation of aspects of ischemia in cell culture: changes in lactate compartmentation.

Aspects of hyperglycemic ischemia were simulated in cultures of astrocytes and of neurons by high glucose and dinitrophenol exposure. Lactate release increased almost sevenfold and it was found that astrocytes were responsible for 92% of the release. There was no significant increase in internal lactate content. Experiments involving loading of astrocytes with lactate at different external pH values showed that lactate accumulation was increased by an increased inward proton gradient. This inward transport of lactate probably consists of two transport components, a passive diffusion of its neutral form and transport via a recently described monocarboxylic acid carrier. It was found that lactate did not get trapped in astrocytes, despite the fact that loading of astrocytes with lactic acid by exposure to 30 mM lactic acid increased the membrane input resistance dramatically. We conclude that lactate is released as lactic acid from astrocytes and equilibrates quickly with all CNS compartments. Thus we argue against a role of lactate accumulation in cytotoxic swelling.

Animals↗

Lactate production and release in cultured astrocytes.

Intracellular lactate content and release of lactate into the surrounding medium of mouse astrocytes in primary culture was measured using the lactate dehydrogenase method. During culturing the cellular content of astrocytes decreased from 400 to 200 nmol/mg protein. The total lactate released into the extracellular space, however, amounted to 75,000 nmol/mg within 98 h, corresponding to a lactate concentration of 10 mM in the cell culture dish. In another set of experiments, cytotoxic swelling was evoked by exposure of the cells to 60 mM K+, this situation caused a 40% increase in cellular volume and an increase in the KCl content of astrocytes. Within 3 h of a change to 60 mM K+ the intracellular lactate content was increased by 100 nmol/mg (one third) and the lactate release in the extracellular space by about 2000 nmol/mg (twice as high as during exposure to 3 mM K+). However, due to the increased intracellular water content, the lactate concentration inside the cells remained unchanged. It is concluded that astrocytes produce substantial amounts of additional lactate during cytotoxic swelling. This lactate, however, is not increasing the intracellular osmolarity and most of the lactate is released into the extracellular space. Depending on the transmembrane transport mechanism it could have the capability to decrease the strong ion difference and contribute to acid shifts in the extracellular space.

Animals↗

Lactate release from cultured astrocytes and neurons: a comparison.

Lactate released into the surrounding salt solution as well as the cellular lactate content were measured in cerebral primary cultures of mouse astrocytes and of mouse neurons. Any newly produced lactate was immediately released as lactic acid into the extracellular compartment via a lactate/proton cotransport. The astrocytic release was about 2,000 nmol x mg-1 x hr-1; the neuronal release was about 300 nmol x mg-1 x hr-1. However, if election transport was blocked with dinitrophenol, the neuronal lactate release was as high as the astrocytic one under normal conditions. High glucose (30 mM) and K+ (60 mM) increased lactate release of astrocytes but not of neurons. In contrast it was found that insulin (1 microM) exposure mainly stimulated neuronal lactate release rather than glial release. Adenosine stimulated both neuronal and glial release. Neither intracellular lactate content nor concentration changed significantly in either cell type under any conditions tested. The pathophysiological implications of these measurements are discussed.

Adenosine↗

KCl movements during potassium-induced cytotoxic swelling of cultured astrocytes.

Astrocytes in primary cultures from mouse cortex were used to investigate the ionic mechanism of cytotoxic swelling which develops after exposure of the cells to 60 mM K+ under isosmotic conditions. Radiotracer analysis combined with a washing efflux method were used to analyze ion changes. We found that both the K+ and the Cl- content increased by about 100% within 1 min after increasing the external K+, and remained constant for 30 min thereafter. The mechanisms, i.e., Na+,K+-ATPase-mediated transport and NaCl/KCl contransport, that are involved in glial ion homeostasis in physiologic situations (extracellular K+ increase to 12 mM) are disturbed in this system and do not contribute to the cytotoxic swelling induced by pathologic K+ concentrations. The Na+,K+-ATPase-mediated K+ uptake is not additionally stimulated by the pathologic K+ increase. The NaCl/KCl cotransport was minimal, presumably due to a severe reduction of the Na+ driving force by the depolarization. The mechanisms of this pathological swelling were found to consist mainly of a passive KCl influx. This influx is mediated by a disturbance of the Donnan equilibrium. It probably involves an increase of the Cl- permeability by activation of a previously described voltage-dependent Cl- channel, which is closed under physiological conditions. However, it was found that the intracellular Cl- accumulation did not completely match the corresponding K+ accumulation. Possible reasons for this anion deficit are discussed.

Animals↗

Mouse placental receptor for basic somatomedin following maternal ethanol administration.

We have previously reported a reduction in the basic somatomedin (B-SM) binding activity of day-15 mouse placental membranes following 3 days of acute maternal ethanol administration. In the present experiments, we have investigated the effects of acute maternal ethanol administration early in gestation on the subsequent development of the placental B-SM receptor, and its relationship to alcohol-related embryofetal growth deficits. Following administration of aqueous ethanol (0.0, 3.6, 5.5 or 7.1 ml/kg) by gavage on days 7, 8 and 9 of gestation, there was no evidence of reproductive impairment in alcohol-treated dams, but there was a significant reduction in day-15 embryonic body weight. Crown-rump length was unaffected. There was no treatment-related difference in the percentage specific binding of [125I]-B-SM by day-15 placental membranes, or in maternal serum B-SM concentrations. These observations suggest that embryofetal growth restriction following maternal ethanol administration is not mediated directly by peripheral unresponsiveness of the B-SM receptor, at least when the exposure occurs early in or prior to placental receptor ontogeny.

Animals↗

The ontogeny of placental Na+-K+ ATPase in the mouse and its impairment by ethanol.

We have investigated the normal ontogeny of Na+-K+ ATPase in the mouse placenta and the possibility that impairment in placental transport capacity, as reflected in reductions in NA+-K+ ATPase activity, is associated with alcohol-related embryonic growth restriction. We have demonstrated that over the normal course of pregnancy there is a dramatic increase in placental NA+-K+ ATPase activity which occurs in concert with the embryofetal body growth spurt. Maternal ethanol administration during the early period of placental enzymogenesis (days 7-9) resulted in a significant reduction (up to 40%) of placental Na+-K+ ATPase activity on day 15. Both the severity and the frequency of the reduction were dose dependent. The effect was associated with significant reductions in embryonic body and brain weight but no change in body length or prenatal mortality. Incubation of term placental fragments for 2 h in increasing concentrations of ethanol resulted in a comparable reduction in enzyme activity. Our studies demonstrate that direct ethanol exposure produces a reduction of placental Na+-K+ ATPase activity, that exposure during the early stages of enzymogenesis results in persistent reductions in Na+-K+ ATPase activity in the mature placenta, and that this effect is associated with deficits of embryonic body and brain growth. A direct causal relationship has not been proven; however, it is conceivable that the correlation between reduced placental Na+-K+ ATPase activity and impaired embryofetal growth reflects a common causal pathway.

Animals↗

Diazepam receptors on mouse astrocytes in primary cultures: displacement by pharmacologically active concentrations of benzodiazepines or barbiturates.

Astrocytes in primary cultures were found to bind large amounts of [3H]diazepam. More than 90% of the total binding is specific, i.e., displaceable by an excess of nonlabeled diazepam. At saturation the specific binding amounts to about 20 pmol/mg protein and the Kd value is 30 nM. Clonazepam and flurazepam displace [3H]diazepam from its specific binding sites; 20-30% displacement is brought about by 0.1-0.3 microM clonazepam, which is similar to the plasma concentrations encountered in epileptic patients treated with this drug. Barbiturates have a similar effect, but considerably higher concentrations are required.

Animals↗

Doxepin, a tricyclic antidepressant, binds to normal, intact astroglial cells in cultures and inhibits the isoproterenol-induced increase in cyclic AMP production.

Doxepin binds to intact astrocytes in primary cultures. The binding is competitively displaceable by excess cold doxepin and it is pronounced (Bmax = 27 nmol/mg protein) but the affinity is rather low (KD = 30 microM). The binding is inhibited by other antidepressants (amitriptyline, desipramine, tranylcypromine, iprindole) and propranolol but not by isoproterenol. Nevertheless, doxepin counteracts effectively the increase in the production of cyclic AMP evoked by isoproterenol.

Animals↗