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Potential energy and spectroscopic constants for the X\(^2 \sum^+ _\mu\) ground state of a;, were calculated by configuration-interaction (Cl) methods, using large basis sets with polarization and diffuse functions. From these CI wavefunctions, the isotropic (a\(_{iso}\)) and dipolar (A\(_{dip}\)) components of the hyperfine coupling constant were obtained. The effects of various s, p basis sets, polarization and diffuse functions, as well as the influence of reference configurations and configuration selection thresholds were investigated. The best values obtained are 35·31 G for a\(_{iso}\) and 29·440 for A\(_{dip}\)• tobe compared with experimental values of 37 ± 1 G and 32 ± 1 G, respectively. It is shown that the contributions to a1so of the K and L shells are opposite in sign, differing by about 4 G. Upon vibrational averaging, both a\(_{iso}\) and A\(_{dip}\) move towards smaller values as v increases. An adiabatic electron affinity of 2·46eV was obtained for CL\(_2\) , and a vertical electron detachment energy of 3·71 eV for Cl;.
Introduction Although symptomatic therapy is available for Parkinson's disease, patients and relatives are faced with continuous severe psychological problems. These psychological problems include: 1. lack of emotional expression, 2. bradephrenia, 3. depression, 4. lack of motivation,S. social anxiety, 6. stress induced increase of symptoms. The first four of these may be at least in part due to the dopamine deficiency. However, even as part of the primary symptoms they have social and communicative impact for patients and relatives. Social anxiety and stress induced increase of symptoms on the other hand clearly result from an interaction of somatic and psychological factors. Social anxiety mainly develops in Parkinson I s disease as an indirect consequence of the motor symptoms. Patients are afraid of being negatively evaluated in the public, of receiving negative comments etc. Thus r social withdrawal increases and the improvement of neurological symptoms following drug treatment may not be fully exploited on the psychosocial level. Stress induced increase of motor symptoms is a commonly observed phenomenon in Parkinson's disease. Even minor stressors, mainly social in nature, can have extreme effects and may elicit or increase tremor or rigidity. A patient can be well in one moment, but unable to move in the next when being aware that he has to leave the house in an hour. Given this situation, patients and relatives have to develop strategies fo~ an emotional balance in the presence of a continuous confrontation with the direct and indirect consequences of the disease. A precondition for developing new psychologically based strategies is an optimwn medical treatment. The integrated approach for neurological and psychological support has the following goals: 1. improving medical treatment for the individual patient, 2. improving psychological coping and psychosocial adaptation for patients and relatives, and 3. evaluating and improving medical and psychological therapy. CONCLUSION Psychological intervention can provide considerable help for a substantial part of Parkinson patients. The main target is coping with stressful social situations. Relaxation and cognitive restructuring together with situational behavioral analysis and training of social skills specifically adapted to the disease are" the main strategies. Various problems remain open at the moment, like the maintenance of motivation which is especially critical for Parkinson patients. Parkins on 's disease is a neurological disease with a known pathological substrate and a therapy which is effective at least for several years on a symptomatic level. The symptoms are tightly connected with psychological emotional and cognitive processes. Moreover, patients and relatives have to cope with symptoms which strongly influence social interaction. And they have to cope together with this situation over a period of ten or twenty years. Thus not only for the patient but also for the health of the relatives, psychological aid is urgently needed. We suggest to integrate psychological approach into the neurological diagnosis and treatment.
We used a sensitive silver degeneration staining method to study the effects of insertion of microdialysis probes in rat dorsal hippocampus and neocortex. Nine animals were sacrificed 24 h, 3 days or 7 days after implantation of dialysis tubing. Although mild neuronal cell death and small petechial hemorrhages were seen in elose proximity to the implantation site, the striking finding was the presence of degenerating axons both adjacent to the implantation site and in remote sites such as the corpus callosum and contralateral hippocampus. The observed changes could alter brain function near or remote from the implantation site and should be considered in analysis of dialysis experiments.
Cardiovascular Effects of Anatoxin-A in the Conscious Rat. SJREN, A.-L., AND FEUERSTEIN, G. (1990). Toxicol. Appl. Pharmacol. 102,91-100. The effects ofanatoxin-A on mean arterial pressure (MAP), heart rate, cardiac index (CI), and blood flow (BF) in hindquarter (HQ), renal (R). and mesenteric (M) vascular beds were studied after intravenous (iv) and intracerebroventricular (icv) administration in the conscious rat. The pharmacological profile of anatoxin-A was further compared to nicotine administered iv and icv. MAP and heart rate were measured from femoral artery, CI by thermodilution method, and blood flow by Doppler velocimetry. Anatoxin-A and nicotine (30, 100 and 300 1-!g/kg iv) produced an increase in MAP with concomitant bradycardia. The highest doses increased Cl. MBF and RBF decreased due to a vasoconstriction in M and R vasculature. These effects were attenuated by the ganglion blocker chlorisondamine (5 mg/kg, iv). Anatoxin-A ( 100 1-!g/k~ iv) increased plasma epinephrine Ievels by 2- fold with virtually no effect on norepinephrine whereas nicotine ( 100 ~oLg/kg, iv) increased plasma epinephrine and norepinephrine by 20- to 30-fold. Central administration of anatoxin-A and nicotine (30-100 ,ug/kg icv) increased MAP with no effect on heart rate and produced M and R vasoconstriction. In summary, the present study demonstrates that anatoxin-A acts as a nicotinic cholinergic agonist in the c.onscious rat after both systemic and centrat administration. Anatoxin-A and nicotine produced pressor and reno-splanchnic vasoconstrictor responses and at high doses increased cardiac output. These effects were mediated by activation ofthe nicotinic receptors in the adrenal medulla and sympathetic ganglia. However, marked differences were found in the potency ofanatoxin-A versus nicotine to stimulate the sympathoadrenomedullary axis.
The transient yellow color observed in the cycloaddition of homobenzvalene (HB) with tetracyanoethylene (TCNE) is associated with the charge-transfer complex [HB, TCNE). The deliberate photoexcitation of [HB,TCNE) affords a mixture of charge-transfer cycloadducts (1, 2, and 3) that differs from that obtained in thermal cycloaddition. The relationship of {HB t TCNE•) radical-ion pair (as the critical reactive intermediate in charge-transfer cycloaddition) to the activation process for thermal cycloaddition is discussed.
4-6-year-old children's understanding of cognitive cuing was studied in 2 experiments using a strategic interaction paradigm. Ghildren could fool a competitor by hiding targets in locations that were labeled with semantically weakly associated cues and help a cooperative partner by hiding them in semantically highly associated locations. Very few 4-year-olds, half the 5-year-olds, and almost all 6-year-olds appropriately chose semantically highly vs. weakly associated hiding places to make the targets easy vs. difficult to find. The second experiment showed that 4-year-olds did not strategically manipulate cues as sources of information, although they themselves proficiently used them as such in a search task. These findings are discussed with regard to research on children's developing understanding of origins of knowledge and belief and with regard to recent claims that young preschoolers possess a metacognitive understanding of cognitive cuing.
The period of natural cell death in the development of rodent motor neurons is followed by a period of sensitivity to axonal injury1-3. In the rat this early postnatal period of vulnerability coincides with that of very low ciliary neurotrophic factor (CNTF) levels in the sciatic nerve before CNTF increases to the high, adult levels4. The developmental time course of CNTF expression, its regional tissue distribution and its cytosolic localization (as suggested by its primary structure)4*5 favour a role for CNTF as a lesion factor rather than a target-derived neurotrophic molecule like nerve growth factor. Nevertheless CNTF exhibits neurotrophic activity in vitro on different populations of embryonic neurons6. To determine whether the vulnerability of motor neurons to axotomy in the early postnatal phase is due to insufficient availability of CNTF, we transected the axons of newborn rat motor neurons and demonstrated that iocal application of CNTF prevents the degeneration of the corresponding cell bodies.
The S fimbrial adhesin (sfa) determinant of E. co/i comprises nine genes situated on a stretch of 7.9 kilobases (kb) DNA. Here the nucleotide sequence of the genes sfa B and sfaC situated proximal to the main structural gene sfaA is described. Sfa-LacZ fusions show that the two genes are transcribed in opposite directions. The isolation of mutants in the proximal region of the sfa gene cluster, the construction of sfa-phoA gene fusions and subsequent transcomplementation sturlies indicated that the genes sfaB and sfaC play a role in regulation of the sfa determinant. ln addition the nucleotide sequence of the genes sfa D, sfa E and sfa F situated between the genes sfaA and sfaG responsible for S subunit proteins, were determined. lt is suggested that these genes are involved in transport and assembly of fimbrial subunits. Thus the entire genetic organization of the sfa determinant is presented and compared with the gene clusters coding for P fimbriae (pap), F1 C fimbriae (foc) and type I fimbriae ( fim). The evolutionary relationship of fimbrial adhesin determinants is discussed.