密盖息治疗49例恶性骨转移瘤疗效观察

目的:观察密盖息(鲑鱼降钙素)的治疗骨转移瘤疼痛和血清钙的临床疗效。方法:单用组用密盖息100IU,肌肉注射,每日2次,共7d。联合化疗组化疗后加密盖息100IU肌肉注射,每日2次,每次7d。治疗结束进行疗效评价。结果:单用组骨痛完全缓解66.7%(12/18)。联合化疗组骨痛完全缓解率87.1%(27/31)。单用组血钙降至正常,占77.8%(14/18),联合化疗组血钙完全降至正常占100%(31/31)。副作用是暂时性的心动过速、皮肤潮红、头晕、恶心呕吐,无需特殊处理,自行缓解。结论:密盖息治疗骨转移瘤有止痛、降低血钙作用良好,副作用小,可以在临床上安全使用。     

Trimellitic anhydride-induced airway syndromes: Clinical and immunologic studies

This report describes a spectrum of respiratory symptoms in workers exposed to trimellitic anhydride (TMA), a biologically reactive chemical used in the plastics industry. Fourteen workers who had worked on a unit which synthesized TMA were evaluated by clinical and immunologic methods. Respiratory syndromes induced by TMA inhalation included asthma and rhinitis of the immediate type, late onset asthma with systemic symptoms, and airway irritation. TMA was shown to couple rapidly to human serum albumin, forming an immunoreactive hapten-protein complex. The workers' immunologic reactivity to this complex could be quantitated and correlated with the three respiratory syndromes. The asthma-rhinitis syndrome was mediated by IgE antibody specific for the TMA hapten. The syndrome of late onset asthma with systemic symptoms was accompanied by elevated levels of TMA-specific IgG antibody. Rheumatoid factor in high titer was found in one worker with IgE-mediated asthma and in two workers with asthma of late onset. Lymphocyte reactivity of TMA-HSA was demonstrated in three workers representative of the three clinical syndromes. Leukocyte histamine release was demonstrated to TMA-HSA in one worker with high levels of IgE antibody specific for TMA-HSA who had severe symptoms of acute rhinitis and asthma.     

Acute neurotoxicity of the Lathyrus sativus neurotoxin, L-3-oxalylamino-2-aminopropionic acid, in the squirrel monkey.

This paper provides the first evidence that the Lathyrus sativus neurotoxin, l-3-oxalylamino-2-aminopropionic Acid (OAP), is toxic when administered intraperitoneally to a primate with a mature bloodbrain barrier. Drowsiness, vomiting, muscle tremors, twitching, convulsions, and death occurred in young male squirrel monkeys (Saimiri sciureus) following injection of 4.26 and 11.4 μmol (0.750 and 2.00 mg) OAP/g body wt. Electroencephalographic changes characteristic of each stage of intoxication were observed. Unchanged OAP was recovered from brain of intoxicated animals. These observations support a possible role for OAP in the etiology of human neurolathyrism, a paralytic disease prevalent among adults in Central India who have consumed large quantities of L. sativus seeds for several months.     

Electrophysiologic effects of atropine on human sinus node and atrium.

Electrophysiologic studies were conducted in 17 patients without apparent sinus node disease before and after intravenous administration of 1 to 2 mg of atropine. Mean values in milliseconds (+/- standard error of the mean) before and after administration of atropine were as follows: sinus cycle length 846 +/- 26.4 versus 647 +/- 20.0 (P less than 0.001); sinus nodal recovery time 1,029 +/- 37 versus 774 +/- 36 (P less than 0.001); mean calculated sinoatrial (S-A) conduction time 103 +/- 5.7 versus 58 +/- 3.9 (P less than 0.001); mean P-A interval 34 +/- 1.5 msec versus 31 +/- 1.5 (P less than 0.05); mean atrial effective and functional refractory periods during sinus rhythm 285 +/- 11.3 versus 238 +/- 7.9 and 331 +/0 11.6 versus 280 +/- 8.6, respectively (P less than 0.001 for both); mean atrial effective and functional refractory periods measured at equivalent driven cycle length 239 +/- 7.7 versus 213 +/- 7.4 and 277 +/- 11.4 versus 245 +/- 9.5, respectively (P less than 0.001 for both). In conclusion, atropine shortened sinus cycle length, sinus nodal recovery time and calculated S-A conduction time. The shortening of atrial refractory periods with atropine implies that vagotonia prolongs atrial refractoriness in man.     

Protective effect of small amounts of glucose on abnormal liver function tests during starvation

The effect of small amounts of oral glucose on hepatic function during starvation was studied. A group of 20, nondiabetic, obese, male patients were entered into the protocol. Ten were placed on absolute caloric starvation and the other ten were placed on a starvation diet modified by the daily addition of 8 or 16 g of oral glucose. Five patients in the starved group crossed over to the modified starvation protocol and 3 of the modified starvation group were switched to the starvation group at the end of the initial dietary period. Total serum bilirubin, serum glutamic pyruvic transaminase (SGOT) and lactic dehydrogenase (LDH) were significantly lower in the modified starvation group compared to the totally starved group. When the groups crossed over the values were similarly altered; the bilirubin and SGOT reduced with the addition of small amounts of glucose and were elevated with starvation. Fasting immunoreactive insulin (IRI), glucagon, and glucose were similar in both groups; but the 90-min postprandial IRI was doubled while only a 15 mg/dl change in blood sugar was seen. The results show that small amounts of oral glucose reduces the total serum bilirubin, SGOT, and LDH elevation of starvation. It is suggested that the postprandial increase in peripheral IRI seen in modified starvation may expose the liver to pulses of portal vein insulin that may exert a protective effect thru the known hepatotrophic effects of insulin.     

Improved tolerance to successive glucose loads in acromegaly.

The mechanism of the Staub-Traugott effect, or facilitated glucose disposal with closely timed successive glucose loads, remains poorly understood. Progressive suppression of growth hormone has been suggested as an explanation. To test this hypothesis, three successive intravenous glucose loads were administered to seven active acromegalic patients and six healthy controls. All subjects showed a clear Staub-Traugott effect despite failure of hyperglycemia to suppress abnormally high growth hormone levels in the acromegalics. Except for higher basal and incremental insulin release in the acromegalic patients, patterns of insulin secretion and suppression of free fatty acids were not substantially different from controls. These studies clearly suggest that hyperglycemia-induced suppression of growth hormone is not the cause of the Staub-Traugott effect.     

Absence of facilitated glucose disposal (Staub-Traugott effect) in subjects with hypopituitarism.

Improved glucose tolerance follows glucose challenges given in rapid succession, the Staub-Traugott effect. The cause for this facilitated glucose disposal is not clear. Augmented insulin release, prior "insulinization" of cells, and suppression of a pituitary factor or free fatty acids (FFA) are previously suggested mechanisms. For information bearing on the role of the pituitary in this phenomenon, study of the Staub effect was undertaken in hypopituitary patients receiving replacement thyroid, cortisone, and sex-steroid therapy and in normal untreated controls. All subjects received three intravenous injections of glucose (0.5 g/kg) at hourly intervals. Plasma glucose, FFA, and insulin were measured. Whereas a definite Staub effect was seen in each control subject, this phenomenon was conspicuously absent in seven hypopituitary patients similarly studied. Patterns of peripheral insulin response were similar for both groups: FFA levels fell more slowly in the hypopituitary subjects. Normal pituitary function appears to be required for the Staub effect. Incremental peripheral insulin levels do not explain the effect. Subnormal suppression of free fatty acids and impaired induction of key glycolytic and glycogenic enzymes are alternative explantations for the absence of the Staub effect in hypopituitary subjects.     

Conduction system examination in a case of spontaneous heart block in a dog

This is a serial-section study of the conduction system in a 2-year-old boxer with electrocardiographic evidence of complete A-V block. The following findings were present: a lack of communication between the atria and the A-V node, atrophy of the A-V node, and tenuous connections between the A-V node and the A-V bundle. These were accompanied by acute degenerative changes in the conduction system. These changes are considered to be the result of arteriolosclerotic heart disease.