Abnormal branching

Fig. 10. Effect of ablation of the Cxi neurons on axon growth from the Til neurons in the grasshopper embryo. (A) Operated leg in which the Cxi neurons had been killed at the onset of Til neuron axonogenesis and the embryo allowed to develop further in culture medium. Asterisk indicates debris of Cxi cells. The Til axons possess multiple abnormal branches (arrowheads). (B) Contralateral control limb for (A) The Til axons take a normal pathway to the CNS. (C) Operated limb bud. The Til axons project straight ahead (arrowhead) towards efferent axons from the CNS, rather than turning posteriorly towards the Cxi cell site. (D) Contralateral control limb bud for (C), showing a normal Ti 1 trajectory. Camera lucida drawings from anti-HRP immunohistochemistry preparations. Scale bar = 100 /tm (reproduced with permission from Nature 304, (1983) Macmillan Magazines Limited).

Pencycuron induces abnormal branching of the hyphae of the sensitive strains of R. solani and its activity is fungistatic [2]. This morphological change implied that the mode of action of pencycuron would be antimicrotubular, like carbenda-zime, and thus it is classified as B4 Cell Division in the FRAC code list. However, while carbendazime inhibits yS-tubuline assembly in mitosis of R. solani, pencycuron does not act there but acts to destroy the cytoskeleton of microtubules. A clear-cut explanation of the mode of action of pencycuron is not yet available. Especially, the mechanistic elucidation as to why pencycuron acts only on quite limited strains of Anastomosis Groups of R. solani remains as an interesting theme. 

The predominance of coronary anomalies is composed of abnormal branching patterns of the proximal segments. CT is therefore used in many instances of suspected coronary anomalies after catheterization angiography to verify or supplement suspected findings. The supplemental function includes visualizing abnormal branches that could either not be reached by the catheter tip during the catheterization procedure or were not at all detected. For this application, CT offers the only way to assess the peripheral parts of that particular branch. Hence, all the restrictions apply as mentioned in the section on initial CAD workup. 

For each branched polymer in this study Ms is obtained from the nominal dimensions of the architecture, in preference to that is influenced by the small number of abnormal branch points in the sample. The values used are given in Table 1. 

Protection is the branch of electric power engineering concerned with the principles of design and operation of equipment (called relays nr protective relays ) which detect abnormal power system conditions and initiate corrective action as quickly as possible in order to return the power system to its normal state. The quickness of response is an essential element of protective relaying systems—response times of the order of a few milliseconds are often required. Consequently, human intervention in the protection of system operation is not possible. The response must be automatic, quick, and should cause a minimum amount of disruption to the power system. 

Glycogenosis type IV (branching enzyme deficiency) results in the formation of a variant of glycogen, characterized by abnormally long inner and outer glucosyl chains and fewer branch points than normal. The abnormal variant is stored in sufficient amounts to cause some vacuolation. The clinical manifestations of this... 

Branching produces highly symmetric structures results in abnormally high melting points. 

Signs Early symptoms include leaves that are yellow, or have a mottled or blotchy appearance. Initial presentation may be on a single shoot or branch but then spreads throughout the tree. Affected trees show twig dieback. Fruit are sparse, small, abnormal in appearance, and fail to color properly. The affected fruit are lopsided, small, and remain green. The fruit often contain aborted seeds. 

Bifunctional protein deficiency. The enzyme defect involves the D-bifunctional protein. This enzyme contains two catalytic sites, one with enoyl-CoA hydratase activity, the other with 3-hydroxyacyl-CoA activity [13]. Defects may involve both catalytic sites or each separately. The severity of clinical manifestations varies from that of a very severe disorder that resembles Zellweger s syndrome clinically and pathologically, to somewhat milder forms. Table 41-6 shows that biochemical abnormalities involve straight chain, branched chain fatty acids and bile acids. Bifunctional deficiency is often misdiagnosed as Zellweger s syndrome. Approximately 15% of patients initially thought to have a PBD have D-bifunctional enzyme deficiency. Differential diagnosis is achieved by the biochemical studies listed in Table 41-7 and by mutation analysis. 

The first leaf symptom of copper toxicity is small yellowish spots that later turn tawny and brownish in color. They are rounded and scattered over the leaf blade without any special pattern, although in some cases spots seem to congregate around the edges and toward the tips of the leaves. Under excessive spraying, leaf tissues show evidence of abnormal hardening, and a crinkle and malformation of the leaf. If the spray is continued, and put on at rather short intervals, a whitish chlorosis exists. In extreme cases defoliation sets in and branches may die. Lowered production would be hardly unexpected. This also has seemed evident from a study of the literature. 

Valine, leucine, and isoleucine are branched-chain amino adds whose metabolism is abnormal in maple syrup urine disease (discussed in Chapter 17). 

Cardiovascular - Ang na pectoris aggravated, arrhythmia, arrhythmia atrial, atrial fibrillation, bradycardia, bundle branch block, cardiac failure, extrasystole, heart murmur, heart sound abnormal, hypertension, hypotension. Ml, palpitation, Q-wave abnormality, tachycardia, ventricular tachycardia (5% or less). 

Hypersensitivity or idiosyncrasy to quinidine or other cinchona derivatives manifested by thrombocytopenia, skin eruption or febrile reactions myasthenia gravis history of thrombocytopenic purpura associated with quinidine administration digitalis intoxication manifested by arrhythmias or AV conduction disorders complete heart block left bundle branch block or other severe intraventricular conduction defects exhibiting marked QRS widening or bizarre complexes complete AV block with an AV nodal or idioventricular pacemaker aberrant ectopic impulses and abnormal rhythms due to escape mechanisms history of drug-induced torsade de pointes history of long QT syndrome. 

Conduction abnormalities Use caution in patients with sick sinus syndrome, Wolff-Parkinson-White syndrome or bundle branch block. 

Again, approximately half of this effect will already be felt at the transition states for insertion and chain transfer. Thus, internal olefins are inserted less easily, oc-branched alkyls are more reactive towards insertion, and secondary alkyls tend to isomerize to primary alkyls. The abnormally low reactivity of Al—Me bonds towards olefin insertion must probably be explained in this way. The high reactivity of (f-Bu)3Al towards ethene insertion, despite its significant steric hindrance, might in part be due to the same effect. 

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