Biomedical subjects
Publications and source records attributed to K C Liang.
A complex case of trisomy 21-related pulmonary hypoplasia with polyhydramnios and hydrops fetalis is described. The value of antenatal surveillance and genetic counselling is emphasized.
Intracerebroventricular infusion of corticotropin-releasing factor (CRF) (0.1-1.0 micrograms) produced a pronounced, dose-dependent enhancement of the acoustic startle reflex in rats. This excitatory effect began about 20-30 min after infusion, grew steadily over the 2 hr test period, and lasted at least 6 hr. Higher doses of CRF (10 micrograms) often produced marked facilitation and then inhibition of startle that oscillated repeatedly with a period of 10-20 min. CRF-enhanced startle did not result from an increase in sensitization produced by repetition of the startle stimulus or from a blockade of habituation. Peripheral injections of the autonomic ganglionic blockers hexamethonium (10 mg/kg) or chlorisondamine (3 mg/kg) slightly attenuated the magnitude of CRF-enhanced startle, suggesting a partial role of peripheral sympathetic activation. Intracerebroventricular infusion of the CRF antagonist alpha-helical CRF9-41 (alpha hCRF; 25 or 50 micrograms) blocked CRF-enhanced startle when infused 5 min prior to CRF, indicating a central site of action. CRF-enhanced startle also was reversed when alpha hCRF was given 90 min after infusion of CRF. This suggests that exogenously applied CRF remains in the brain for a very long time after administration or that CRF given exogenously initiates a process that results in a long-lasting activation of endogenous CRF. Because the startle reflex is elevated by both conditioned and unconditioned fear, these data lend further support to the idea that CRF infusion produces a behavioral state that resembles fear or anxiety. Because startle is mediated by a well-defined neural pathway, CRF-enhanced startle may provide a useful behavioral assay to analyze the neural systems upon which exogenous CRF acts to produce its behavioral effects.
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Intracerebroventricular (icv) infusion of corticotropin-releasing factor (CRF) was previously found to produce a long-lasting, dose-dependent (0.1-1.0 microgram) increase in the amplitude of the acoustic startle reflex. The present study sought to determine where in the CNS CRF acts to increase startle. Intracisternal infusion of CRF (0.1-1.0 microgram) increased startle with a time course and magnitude similar to that produced by icv CRF, unlike intrathecal infusion, which produced a small, more rapid enhancement of startle. While lesions of the paraventricular nucleus of the hypothalamus had no effect on icv CRF-enhanced startle, bilateral lesions of the central nucleus of the amygdala significantly attenuated the excitatory effect of icv CRF but had no effect on intrathecal CRF-enhanced startle. Even though lesions of the amygdala blocked icv CRF-enhanced startle, local infusion of CRF into the amygdala did not significantly elevate startle. The present data indicate that the amygdala is part of the neural circuitry required for icv CRF to elevate startle, but does not appear to be the primary receptor area where CRF acts. The involvement of the amygdala in icv CRF-enhanced startle is consistent with the hypothesis that both the amygdala and CRF are critically involved in fear and stress.
Malaria had been a very serious endemic disease in Taiwan before it was eradicated. There has been a long history of struggle against this disease since the beginning of this century. A large scale chemotherapy program was initiated in 1910 following Koch's method. The inhabitants in the highly malarious area were subject to monthly blood examination and those positive for malaria parasites were compulsorily treated with antimalaria drugs. This program was continued until 1944. Malaria transmission was not interrupted, but the parasite rate among the inhabitants included in the program was maintained at 2% to 3% level for 35 consecutive years, and the number of deaths caused by malaria was brought down gradually from an average of 36 per 10,000 population before 1910(1906-1909) to less than 8 in the 1930s. Throughout the history of malaria control in Taiwan, other control measures were also applied. They were: personal protection, source reduction and antilarval operations. All these methods were proven to be effective, but with limitations. The availability of DDT and other residual insecticides in the 1940s marked a new era for malaria control in the world, as well as in Taiwan. A 6-year malaria eradication program using the DDT residual house spraying method was launched in 1952 and then followed by vigorous malaria surveillance activities which finally eliminated all the remaining foci of transmission. In 1965, Taiwan was registered by the World Health Organization on its list of countries where malaria eradication has been achieved. Although there has been no indigenous malaria in Taiwan, cases have been imported continuously from abroad. In the last 25 years, with the painstaking vigilance efforts, the malaria-free status has been maintained. It is hoped that these efforts will be continued so that malaria will never again come back to Taiwan as an endemic disease.
These experiments examined the role of two major amygdala afferent-efferent pathways--the stria terminalis (ST) and the ventral amygdalofugal pathway (VAF)--in mediating the effects, on memory storage, of post-training intra-amygdala injections of norepinephrine (NE) and subcutaneous (s.c.) injections of epinephrine (E). Rats with either ST lesions or VAF transections and sham-operated rats were trained on a one-trial step-through inhibitory avoidance task and immediately after training received intra-amygdala injections of NE or a buffer solution. Other groups of VAF-transected animals received post-training s.c. injections of E or saline. ST lesions blocked the memory-enhancing effect of intra-amygdala injections of a low dose of NE (0.2 microgram) as well as the amnestic effect of a high dose of NE (5.0 microgram). In contrast, VAF transections did not block the memory-enhancing effect of NE (0.2 microgram). However, VAF transections attenuated the memory-enhancing effect of s.c. injections of E: the effective dose of E was shifted from 0.1 to 0.5 mg/kg. These findings, considered together with previous evidence that ST lesions block the memory-enhancing effect of peripheral E injections, suggest that the VAF is involved in mediating the central influence of peripheral E on amygdala functioning, while the ST is involved in mediating amygdala influences on memory storage elsewhere in the brain.
In a study of 82 cases of clinical chorioamnionitis in which no antibiotics were administered antenatally, significant villous edema was observed in 51 placentas (62%). Polymorphonuclear leukocyte invasion of the placental plate was found in 53 placentas (65%). The presence of SVE was significantly associated with placental bacterial recovery, occurrence of prolonged rupture of membranes, lower one minute Apgar score, the need for resuscitation and significant neonatal respiratory problems. Findings suggest that bacteria-related placental villous edema can lead to significant perinatal and neonatal morbidities.
Seventy-eight women at earlier than 35 weeks' gestation with premature rupture of membranes and/or preterm labor were randomly assigned to receive either 10 mg vitamin K1 intramuscularly (IM) or no treatment. If delivery did not occur within 4 days, the dose of vitamin K1 was repeated. Women whose pregnancies continued beyond 8 days received 20 mg of vitamin K1 orally every day until the end of the 34th week or until delivery, whichever occurred earlier. The median maternal plasma vitamin K1 level was significantly higher in treated than in untreated subjects (11.592 versus 0.102 ng/mL; P less than .001). The median cord plasma levels were 0.024 ng/mL in the treated group and 0.010 ng/mL in the controls, a significant difference (P = .046). Median plasma vitamin K1 levels were comparable in mothers receiving the drug by the IM route only and by both the IM and oral routes (10.533 versus 11.928 ng/mL; P = .460). The infants of the latter group, however, had significantly higher median cord plasma levels (0.42 versus 0.017 ng/mL; P less than .001). There was no correlation between cord plasma vitamin K1 levels and gestational age or duration of maternal supplementation with vitamin K1. We conclude that, in preterm pregnancies, vitamin K1 crosses the placenta slowly and to a limited degree.
The effect of maternal administration of vitamin K1 on cord blood prothrombin time, activated partial thromboplastin time, activity of factors II, VII, and X, and antigen levels of factors II and X in infants less than 35 weeks' gestation was evaluated. Pregnant women in preterm labor were randomly assigned to receive 10 mg of vitamin K1 intramuscularly or no injection. If delivery did not occur in 4 days, the dose of vitamin K1 was repeated. Women who continued their pregnancy 4 days beyond the second dose received 20 mg of vitamin K1 orally daily until the end of the 34th week of gestation. The birth weights of infants ranged from 370 to 2550 g and gestational age ranged from 22 to 34 weeks. The prothrombin time, activated partial thromboplastin time, factors II, VII, and X activity, and factors II and X antigen levels were not statistically different in either group of infants. Intraventricular hemorrhage occurred in 25 of 51 control infants and 25 of 47 vitamin K-treated infants. More control infants had grade III intraventricular hemorrhage on day 1 (P = .032), but on day 3 and 14 of life, the severity of intraventricular hemorrhage was comparable in both groups. Infants in whom an intraventricular hemorrhage developed were significantly smaller, younger, and more critically ill than infants without intraventricular hemorrhage. Administration of vitamin K1 to pregnant women at less than 35 weeks' gestation does not improve the hemostatic defects nor does it reduce the incidence or severity of intraventricular hemorrhage in their infants.
The effects of intra-amygdala injections of corticotropin-releasing factor (CRF) on memory and exploratory behavior in rats were examined in the present study. Rats with chronically implanted cannulae received intra-amygdala injections of vehicle or CRF at a dose of 0.01, 0.1 or 1.0 micrograms, either immediately after the inhibitory avoidance training or prior to the open field activity test. Results indicated that while CRF at low (0.01 microgram) and high (1.0 micrograms) doses produced no significant effect on retention or exploration, immediate post-training intra-amygdala injections of CRF at the medium dose (0.1 microgram) significantly improved retention of the inhibitory avoidance response. The same dose of CRF, given shortly prior to the open field activity test, decreased locomotor activity, rearing and hole-poke responses in rats. These results suggest that the amygdala is one of the anatomical loci involved in CRF modulation of memory processing and exploration in rats. The implication of CRF in mediating the influences of stress on behavior is discussed.
Thoracic spinal cord transection below the origin of the brachial plexus is a rare event among breech-presenting infants delivered by cesarean section. A case of a thoracic (T3-T4) spinal cord injury with paravertebral hemorrhage mimicking catastrophic intracranial bleeding is presented to illustrate the value of careful application of traction or any longitudinal stretching forces during fetal head extraction.
These experiments examined the effects, on retention, of posttraining intra-amygdala administration of norepinephrine (NE), and propranolol. Rats were trained on a one-trial step-through inhibitory avoidance task and tested for retention 24 h later. Injections were administered bilaterally (1.0 microliter/injection) through chronically-implanted cannulae. Low doses of NE (0.1 or 0.3 microgram) administered shortly after training enhanced retention while higher doses (1.0 or 5.0 micrograms) were ineffective. Retention was not affected by NE administered 3 h after training. The effect of intra-amygdala NE on retention is blocked by simultaneous administration of propranolol (0.2 microgram). This finding suggests that the memory-enhancing effect of NE may be mediated by beta-receptors. Posttraining intra-amygdala NE also attenuated the retention deficit produced by adrenal demedullation. Further, intra-amygdala injections of propranolol (0.2 microgram) blocked the enhancing effect, on retention, of posttraining s.c. injections of epinephrine. These findings suggest that activation of noradrenergic receptors in the amygdala may be involved in memory processing and may play a role in the memory-modulating effect of peripheral epinephrine.
Amygdala stimulation produces a robust retrograde amnesia which appears to be related to peripheral hormonal responses to stress. This present study investigated the effects of electrical stimulation of the amygdala delivered immediately after inhibitory and active avoidance training to rats depleted of adrenal catecholamines or sham adrenal operated rats. Comparable findings were obtained with the two training tasks: amygdala stimulation impaired retention of sham adrenal operated rats but it enhanced retention of rats depleted of adrenal catecholamines. These findings suggest that adrenal catecholamines released during a training situation modulate the effects of amygdala stimulation on memory.
The present study investigated the role of adrenal epinephrine in the memory modulatory effects of post-training amygdala stimulation. Adrenal demedullated (ADMX) or sham demedullated (SHAM) rats received electrical stimulation of the amygdala immediately after training on inhibitory and active avoidance tasks. With both tasks, the stimulation impaired retention only in the rats with intact adrenal medullae: the retention performance of the ADMX in the rats with intact adrenal medullae: the retention performance of the ADMX rats given post-training stimulation was better than that of the unstimulated ADMX group with implanted electrodes. However, ADMX rats given post-training epinephrine (1.0 mg/kg, s.c.) immediately before the amygdala stimulation had retention deficits comparable to those of the SHAM group given amygdala stimulation. If epinephrine was administered a short time after rather than before the post-training amygdala stimulation, retention of the ADMX animals was not impaired. The findings are interpreted as indicating that circulating epinephrine present at the time of amygdala stimulation modulates the effects of amygdala stimulation on memory.
The present study investigated the involvement of two amygdala pathways, the stria terminalis (ST) and the ventral amygdalofugal pathway (VAF), in the effect of post-training electrical stimulation of the amygdala on retention. Rats with implanted amygdaloid electrodes and ST lesions, VAF transections or sham pathway operations, were trained on an inhibitory avoidance task and an active avoidance task. Electrical stimulation of the amygdala was given immediately after training and retention was tested 24 h later. In rats with sham ST lesions, post-training amygdaloid stimulation impaired retention in both tasks. Lesions of the ST did not significantly affect retention in the unstimulated rats. However, the ST lesions attenuated the amnestic effect of amygdaloid stimulation. In rats with sham VAF transections, stimulation of the amygdala impaired retention in the inhibitory avoidance task but enhanced retention in the active avoidance task. Transecting the VAF impaired retention performance of the unstimulated rats in the inhibitory avoidance task. However, the VAF transections did not alter the effect of amygdaloid stimulation: in both tasks, the retention performance of stimulated rats with VAF transections did not differ from that of stimulated rats with sham transections. These findings suggest that the ST may be involved in mediating the influences of the stimulated amygdala in modulating memory storage processing in the brain.
This study investigated the effect of naloxone on amnesia produced by subseizure amygdaloid stimulation. Animals were trained in an inhibitory avoidance task, and given amygdaloid stimulation following training. Immediately after training, prior to stimulation, naloxone was injected either peripherally (i.p.) or into the bed nucleus of the stria terminalis (BNST) where the Met-enkephalin-containing fibers from the amygdala terminate. Amygdaloid stimulation caused retention deficits. The deficits were attenuated by 3.0 mg/kg naloxone given peripherally or by 1.0 microgram or 0.3 microgram naloxone injected bilaterally into the BNST. The attenuative effect was anatomically and receptor specific: 0.3 microgram of naloxone injected into the caudate nucleus was ineffective; the attenuative effect of naloxone was antagonized by simultaneous injection of 1.5 or 4.5 micrograms levorphanol into the BNST. These results suggest that endogenous opioids, possibly the enkephalins of the stria terminalis released into the BNST following amygdaloid stimulation, are at least partially involved in mediating the effect of amygdaloid stimulation on memory.
Bilateral subseizure stimulation of the amygdala given immediately following training in an inhibitory avoidance task produced retrograde amnesia. Hexamethonium (3.0 and 10.0 mg/kg), a peripherally acting nicotinic cholinergic antagonist, attenuated the retention deficits induced by amygdala stimulation if the drug was given 30 min prior to, but not immediately following training. Hexamethonium had no effect in normal unoperated animals, but did produce a retention deficit in operated control (nonstimulated) animals if it was given immediately following training (3.0 and 10.0 mg/kg). The results suggest that memory deficits induced by electrical stimulation of the amygdala are associated with, or perhaps mediated in some way by peripheral autonomic function.
This study investigated the effect of the stria terminalis (ST) lesions on the retention facilitation produced by post-training epinephrine. Rats with sham or bilateral ST lesions were trained on a one-trial step-through inhibitory avoidance task and, immediately after training, received saline or one of 3 doses (0.01, 0.1 or 1.0 mg/kg, s.c.) of epinephrine. In the rats with sham ST lesions, all 3 doses of epinephrine significantly enhanced retention performance. Lesions of the ST did not affect retention significantly. However, the lesions attenuated the facilitating effect of epinephrine on retention. These findings suggest that the integrity of the ST, which connects the amygdala and other brain structures, is essential for the effect of epinephrine on memory processes. The possible involvement of the brain structures processing visceral information in the memory modulatory effect of epinephrine is discussed.