Finger ridge patterns in psoriasis.
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Biomedical subjects
Publications and source records attributed to S Lal.
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A single fasting level of serum prolactin was measured in each of sixty control subjects and eighty-three psychiatric patients of both sexes who had been on neuroleptic therapy for 2-4 weeks (acute treatment) or at least 5 years (chronic treatment) and who were aged either 17-45 or 48-85 years. All groups of patients had significantly higher mean prolactin levels than controls. Gender, age group of women, and exposure to acute or chronic treatment were significant variables determining the magnitude of neuroleptic-induced elevation of prolactin. In some of the groups, dose, duration of chronic therapy, and concomitant administration of anticholinergic drugs also influenced prolactin levels. Whereas all acutely treated women had prolactin values above the control range, one out of twelve (8-3%) of the women aged 17-45 years and six out of fourteen (42-9%) of the women aged 48-85 years who were under chronic treatment had normal values. Normal prolactin levels were also found in five out of sixteen (31-2%) of the acutely treated and nine out of twenty-four (37-5%) of the chronically treated men aged 17-85 years.
Tryptophan was measured in the ventricular CSE and serum and the neutral amino acids leucine, isoleucine, valine, phenylalanine, and tyrosine were measured in the serum of two cases with ventricular drains. Samples were taken every two hours for 24 hours in one case and for 16 hours in the other. The CSF tryptophan was correlated significantly with the free--that is, non-albumin-bound--serum tryptophan but not with the total serum tryptophan. CSF tryptophan was not correlated significantly with the ratio of free serum tryptophan to the sum of the neutral amino acids. These data suggest that, in man, brain tryptophan concentrations are influenced by the free and not the total serum tryptophan and that physiological variations of the neutral amino acids do not appreciably influence the concentration of brain trytophan.
Adenosine 3', 5'-monophosphate (cAMP) was measured in the CSF of 42 patients undergoing radiological investigation, neurosurgical procedures, or investigation of hepatic coma. The concentration of cAMP was significantly higher in ventricular CSF than in lumbar CSF. Premedication with pentobarbitone plus promethazine increased cAMP in lumbar CSF. There was no difference in cAMP concentration in lumbar CSF obtained before or after injection of air or after the administration of diazepam during lumbar pneumoencephalography. Lumbar CSF cAMP concentration was significantly increased in patients in hepatic coma. The concentration of cAMP in the lateral ventricle was not affected by general anaesthesia or by the presence of a complete block of the aqueduct of Sylvius. There was no decrease in lumbar CSF cAMP in patients with a complete stenosis of the aqueduct of Sylvius, partial blocks of CSF flow at the cervical level, or a complete block at the lower thoracic level. The concentration of cisternal CSF cAMP was similar to that of lumbar CSF. These results suggest that (1) there is a ventriculolumbar gradient in the concentration of cAMP but of insufficient magnitude to be detected by mixing of lumbar and ventricular CSF during pneumoencephalography, (2) lumbar CSF cAMP concentration is not dependent on brain as a source of this nucleotide; the source of this nucleotide may be largely derived from the spinal cord, (3) premedication may affect the concentration of cAMP in lumbar CSF cAMP, (4) the formation of cAMP is unimpaired in hepatic coma.
Serum growth hormone (GH) and prolactin (PRL) concentrations were measured after administration of the dopamine receptor agonist, apomorphine HC1 (0.75 mg subcutaneously), to 17 chronic schizophrenic patients, four of whom had an oral dyskinesia, who were withdrawn from chronic neuroleptic therapy for periods of two to 15 weeks, and in 21 control subjects (normal volunteers or physically healthy alcoholics not exposed to neuroleptics). Six of the schizophrenic patients, but none of the controls, had raised baseline levels of GH (greater than 6 ng/ml). After apomorphine all controls showed an increase in serum GH with a peak concentration of 9 ng/ml or more, whereas eight subjects withdrawn from neuroleptics showed an inadequate response (peak less than 6 ng/ml) and in two others an inadequate response was obtained on one of two trials. The peak GH concentration was significantly less after apomorphine in patients withdrawn from neuroleptics (11.90 +/- 3.19 ng/ml) compared with controls (20.80 +/- 2.11 ng/ml) (P less than 0.05). Among patients withdrawn from neuroleptics, those with an oral dyskinesia had significantly lower peak GH concentration 2.46 +/- 0.93 ng/ml) after apomorphine compared with those without (14.85 +/- 3.83 ng/ml) (P less than 0.05). There were no differences in serum PRL concentrations, before or after apomorphine administration, between patients withdrawn from neuroleptics and controls. In uncontrolled observations none of the four patients with an oral dyskinesia showed any worsening of the movement disorder after apomorphine. These data provide no evidence for supersensitivity of dopamine receptors in chronic schizophrenic patients withdrawn from chronic neuroleptic therapy.
A follow-up study is reported of a consecutive series of 360 women who underwent termination of first trimester pregnancies by vacuum aspiration. Each patient received brief counselling before termination. Follow-up examinations were carried out by means of detailed, structured interviews at three months and between 15 months and two years (mean: 18 months) after termination. Outcome was assessed in terms of psychiatric symptoms, guilt feelings, and adjustment in marital and other interpersonal relationships, sexual responsiveness and work record. Compared with ratings of psychosocial adjustment before termination, significant improvement had occurred at follow-up in respect of psychiatric symptoms, guilt feelings and interpersonal and sexual adjustment; there was no significant change in marital adjustment. Adverse psychiatric and social sequelae were rare.
The time-course of apomorphine in brain was studied in 7-day-old and young adult rats following i.p. injection of 10 mg/kg apomorphine. In the adult animals continuous stereotypes behaviour (SB) commenced within 1-2 min and was no longer present at 75 min. The peak concentration of apomorphine was present at 5 min and then declined exponentially (half-life = 10.5 min); only trace amounts (less than 0.01 mug/g) were present at 90 min. In the immature rat apomorphine induced an initial phase of intermittent locomotion lasting about 10 min after which the rats appeared sedated; 60-80 min after injection intermittent SB emerged and terminated 150-180 min after the apomorphine injection. The peak brain concentration of apomorphine was present at 10 min and then declined exponentially (half-life = 28 min). Significant amounts of apomorphine were still present in brain at 150 min and trace amounts evident at 180 min. The reason for the delayed onset of SB in the immature rat is unclear. The longer half-life is presumably related to incomplete development of enzyme systems metabolizing apomorphine in the immature animal.
The case of a 40 years male suffering from post-kala-azar dermal leishmaniasis simulating nodular lepromatous leprosy is reported. In countries where leprosy is endemic, other diseases are not infrequently taken to be leprosy (Schaller, 1971). Dermal leishmaniasis is a common cause of confusion in countries where the condition is endemic (Browne, 1964). Dharmendra and Chatterji (1940) discussed in detail the question of differential diagnosis between Leprosy and Dermal Leishmaniasis. The present communication is concerned with a patient suffering from post-kala-azar dermal leishmaniasis whose skin lesions simulated nodular lepromatous leprosy.
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