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Es wird über den Fall einer hochgradigen Deformität der thorakolumbalen Wirbelsäule nach Resektion eines Sarkoms berichtet. Nach adjuvanter Radiatio bestand ein ausgedehnter Strahlenschaden im Bereich der Haut mit chronischer Fistelung. Es erfolgte die Korrektur über eine Closing-Wedge-Osteotomie von L3 und Verlängerung der vorhandenen dorsalen Instrumentierung (Th10-L4) auf Th8 und das Os ileum. Am Folgetag erfolgte eine Weichteildeckung durch eine freie Latissimus-dorsi-Lappenplastik, welche an eine arterio-venöse Gefäßschleife in der Axilla angeschlossen wurde. Durch dieses interdisziplinäre Vorgehen konnte eine nahezu vollständige Korrektur und eine sichere Weichteildeckung erreicht werden. This article presents the case of a high-grade deformity of the thoraco-lumbar spine. The patient suffered from a sarcoma that was radically resected. Due to adjuvant radiation, the patient suffered from a radiation injury with chronic fistula. In a two-stage approach, the deformity was corrected by a closing-wedge osteotomy of L3 with elongation of the present dorsal spondylodesis (Th10-L4) to Th8 and the iliac bone. Soft-tissue reconstruction was achieved by a free latissimus dorsi flap that was anastomosed to an axillary arterio-venous loop. The presented interdisciplinary approach allowed an almost complete correction of the deformity and stable soft-tissue coverage.

The following case report describes a Burmese subject with an unusual birthmark and birth defects thought by local people to be linked to events surrounding the death of his mother's first husband. The nature of the link is explored, including how the assumption of a linkage could have led to subsequent events.

Patients who died of a melanoma thinner than 1.5mm within 96 months (group 1, n=60) were compared with those having a tumor of the same thickness who had not died in this time period (Group 2, n=300). Both groups were investigated with respect to differences in patients sex and age and to thickness, diameter, exophytic growth, and site of the melanoma as well as the number of mitoses/mm2 of tumor area. Relatively speaking, more men than women died of a thin melanoma: in Group 1 (deceased) there were 32 men and 28 women, in Group 2 (alive) 58 men and 242 women. The better survival rate of females did not depend on the difference in the predominating melanoma locations (?face and legs; ? trunk): in both sites, on the legs and on the trunk, women had a significantly higher 8-year survival rate than men with equally thick tumors. Furthermore, melanomas on the arms and legs of females had a better prognosis than those on the trunk and face. Both the patient's sex and the tumor site seem to influence the survival of melanoma patients. Only in men was the median of mitoses/mm2 of tumor area found to be higher in the first group (2.2) than in the second group (0.75). In women, no marked difference in the mitotic count was found (Group 1:1.1; Group 2:1.15).

The entire operon coding for the enzymes responsible for conversion of toluenes to benzoates has been cloned from TOL plasmid pWW53 and the position of the genes accurately located. The coding region was 7.4 kilobase pairs (kbp) long, and the gene order was operator-promoter region (OP1)-a small open reading frame-xylC (1.6 kbp)-xylA (2.9 kbp)-xylB (1.8 kbp). Within the coding region there was considerable homology with the isofunctional region of the archetypal TOL plasmid pWW0. A central region of 2.9 kbp complemented an xylA (for xylene oxygenase) mutant of Pseudomonas putida mt-2 and was also capable of conferring the ability to convert indole to indigo on strains of Escherichia coli and P. putida. This reaction has been reported previously only for dioxygenases involved in aromatic catabolism but not for monooxygenases. It is proposed that the region encodes xylene oxygenase activity capable of direct monohydroxylation of indole to 3-hydroxyindole (oxindole), which then spontaneously dimerizes to form indigo.

Pseudomonas putida MT53 contains a TOL plasmid, pWW53, that encodes toluene-xylene catabolism. pWW53 is nonconjugative, is about 105 to 110 kilobase pairs (kbp) in size, and differs significantly in its restriction endonuclease digestion pattern and incompatibility group from the archetypal TOL plasmid pWW0. An RP4::pWW53 cointegrate plasmid, pWW53-4, containing about 35 kbp of pWW53 DNA, including the entire catabolic pathway genes, was formed, and a restriction map for KpnI, HindIII, and BamHI was derived. The entire regulated meta pathway genes for the catabolism of m-toluate were cloned into pKT230 from pWW53 on a 17.5-kbp HindIII fragment. The recombinant plasmid supported growth on m-toluate when mobilized into plasmid-free P. putida PaW130. A restriction map of the insert for 10 restriction enzymes was derived, and the locations of xylD, xylL, xylE, xylG, and xylF were determined by subcloning and assaying for their gene products in both Escherichia coli and P. putida hosts. Good induction of the enzymes by m-toluate and m-methylbenzyl alcohol but not by m-xylene was measured in P. putida, but little or no regulation was found in E. coli. The restriction map and the gene order showed strong similarities with published maps of the DNA encoding both the entire meta pathway operon (xylDLEGFJIH) and the regulatory genes xylS and xylR on the archetype TOL plasmid pWW0, suggesting a high degree of conservation in DNA structure for the catabolic operon on the two different plasmids.

Pseudomonas putida MT15 contains a 250-kilobase-pair (kbp) TOL plasmid pWW15, encoding toluene and xylene catabolism, which undergoes large spontaneous deletions to give two classes of mutants with altered catabolic phenotypes (H. Keil and P. A. Williams, J. Gen. Microbiol, 131:1023-1033, 1985). Two structural genes for catechol 2,3-oxygenase (C23O) were cloned from pWW15. The gene for C23OI was located on the 2.1-kbp XhoI fragment Xh, whereas that for C23OII was found on the 11.5-kbp BamHI fragment BJ. The two restriction fragments and the subcloned regions of them showed no similarity in the pattern of restriction digestion, nor did they hybridize with each other. The substrate specificities of the two enzymes were also substantially different. The two structural genes were separated on pWW15 by about 100 kbp. In plasmid pWW15-510 of a B5 mutant, the 90-kbp deletion in the plasmid removed most of the intervening DNA, but it also deleted 80% of the gene for C23OI from its 3' end. Thus, only C23OII was expressed in the host MT15-510. Conversely, in RP4::pWW15 cointegrate plasmid pWW15-1003, only the C23OI gene was present. The expression of C23O activity from these two derivative plasmids and from the wild-type pWW15 showed that only C23OI was induced by growth in the presence of m-toluate, whereas both activities were induced in the only C23OI was induced by growth in the presence of m-toluate, whereas both activities were induced in the presence of m-xylene. These findings cast doubt on the earlier hypothesis that the deletions in B3 and B5 mutants remove a regulatory gene by which m-toluate induces the enzymes necessary for its own catabolism.

Waddell, Steenbock, Elvehjem, and Hart1showed that rats fed milk exclusively developed nutritional anemia and that the ingestion of pure iron salts failed to cure it. However, normal regeneration of hemoglobin was obtained with small additions of copper sulphate along with the iron salt. These results have been confirmed by Keil and Nelson.2Myers and Beard3found that higher doses of zinc and magnesium retarded blood regeneration. If this is the case, anemia should develop more rapidly on milk and FeCl3if these elements are included. The slope of the curves obtained with and without zinc or magnesium demonstrate that anemia resulted as readily with or without these elements.Prior to this work on hemoglobin regeneration, Daniels and Hutton4demonstrated that rats failed to reproduce on milk and iron, but reproduction was a success when a mineral mixture of NaI, NaF, KAl (SO4)2, MnSO4, and Na2SiO3was added. They concluded that all of these salts were necessary in the milk for reproduction. The work of Hart, Steenbock and associates1and Keil and Nelson2is so conclusive, that it is certain animals cannot grow and reproduce normally without copper. There must have been contamination of this element either in the milk or salt mixture used by Daniels and Hutton. The minimum amount of copper required for regeneration of hemoglobin is extremely small. The minimum amount of copper as CuSO4, when injected intraperitoneally, is shown to be 0.002 mg. daily. The milk used in these experiments was collected directly into glass containers in order to avoid contamination with copper. Milk ad liband 0.5 mg. of Fe as FeCl3daily were fed to the rats. 0.05 mg. of Fe as FeCl3injected intraperitoneally with 0.002 mg. Cu as CuSO4daily does not result in normal regeneration.

The difficulties in providing additional information which assists in the interpretation of significance levels are discussed. The possibility of providing empirical data is suggested by investigating the probable occurrence and actual detection of Type I and Type II errors in a survey of past research activities. Dealing with exceptions, initial small scale results cannot be easily provided but a suitable large scale inquiry conducted for other purposes, may provide a starting point.

SINCE 1962 several investigators have reported experimental results supporting the claim that Pavel Stepanek of Prague could demonstrate an ESP ability in a simple test situation. In the test used, Stepanek attempted on each trial to say whether the green or the white side of a card hidden in an opaque cover was presented upward. Two of us1summarized the literature dealing with this subject and presented confirmatory evidence obtained in stringently safeguarded experimental conditions.

This work is the outgrowth of the studies made by the authors on the relation of iron and copper to nutritional anemia and hemoglobin synthesis. It is well known that cow's milk is inadequate for the normal maintenance of the rat. Additions of copper and iron salts to an exclusive milk diet protect animals from nutritional anemia and produce an apparent well being in the animals of the first generation from the standpoint of hemoglobin formation, growth, and reproduction. Underhill, Orten, Mugrage, and Lewis1have observed no abnormalities in the organs of rats fed milk, copper, and iron for periods of more than a year. Waddell2reported sterility in males of the first generation receiving a milk, copper, and iron diet. The sterility was marked by a progressive testicular degeneration together with an absence of motile sperm in the seminal fluid. Ferric chloride, when added to the ration, was found to produce symptoms of sterility as early as 10 weeks after administration. Keil, Keil, and Nelson3found the animals on a milk, copper, and iron ration grow more slowly than those on a good stock diet. Reproduction occurred in animals of the first generation, but the second generation did not reproduce. Our results on second generation rats, together with the findings of Waddell, led us to investigate both males and females of the first and second generations in order to ascertain whether or not the sterility on this diet could be ascribed to degeneration of sex organs.All of the animals (rats) were fed whole milk obtained from Holstein cows in the dairy herd at Iowa State College. The milk was collected directly into glass jugs, in order to avoid contmination with inorganic substances.

All of the experiments were performed on rats. The animals were made anemic by feeding whole milk, collected in glass containers. The materials studied for hemoglobin regeneration were all tested for copper and used only when this element was absent. Hemoglobin was determined by the Newcomer method. The animals were bled by the tail.There was no effect on hemoglobin when anemic rats were fed 1, 5, and 10 mg. Fe as FeCl3together with whole milk. We then studied the effect of tyrosine, tryptophane, glutamic acid, aspartic acid, and arginine on hemoglobin formation. The rats were fed on milk when 30 days old and after 4 weeks were given 100 mg. of amino acid plus 0.5 mg. of Fe as FeCl3daily. Regeneration of hemoglobin did not occur on any of the amino acids employed. The conflicting results in the literature on the potency of various elements in hemoglobin building may be due to different amounts being absorbed; to test this point we injected various salts intraperitoneal-ly. The following elements were tested: As, Mn, V, Ge, Ni, Zn, Cr, Ti, Se, Hg, and Rb. Most of the metals were injected at levels from 0.05 mg. to 0.1 mg. daily. Arsenic was injected at 0.01 to 0.2 mg. daily. None of these elements caused regeneration of hemoglobin; in fact, the only element we have thus far found which has a positive effect is copper. Although we found that Fe as FeCl3when administered orally did not stimulate hemoglobin regeneration, we were anxious to ascertain if the same results would be obtained by intraperitoneal injection of the Fe. Three mg. of Fe as FeCl3injected every other day into anemic rats increased the hemoglobin from initial levels of 3.0 to 5.5 gm. to final values of 9.5 to 12.1 gm. per 100 cc. of blood.

TO THE EDITOR:— In the March issue of the Archives of Dermatology and Syphilology (31:371, 1935), Montgomery recorded a case in which there occurred simultaneously lesions of lupus erythematosus and an eruption resembling lichen scrofulosorum; on the basis of this association, it was adduced that the former dermatosis is a tuberculid. Naturally, I am interested in such instances since they would tend to negate the conclusions which I drew from a study of the postmortem data in over 125 cases of the disease. Further necropsy studies (about 50 personally observed cases) have corroborated and strengthened my belief that there is no direct relationship between lupus erythematosus and tuberculosis.In reviewing my paper for the 1934 "Year Book of Dermatology," Wise and Sulzberger, although not openly professing a belief in the relationship of the two conditions, did what all the adherents of this theory must now do to support the

The hemoglobin value of the blood of rats on our growing ration varies from 15 to 18%. The hemoglobin content of the blood of rats on whole milk falls to 2 to 5% in 10 weeks. The females respond to anemia and die sooner than the males. Ferric chloride increased the hemoglobin to 16% in 9 weeks. The ferric chloride was made from high grade standardization iron wire. The wire was dissolved in pure HCl to which was added a small amount of pure HNO3, and H2S was bubbled through the diluted solution to precipitate any copper present. The chloride was then crystallized. The Hilger spectrograph showed no copper in the ferric chloride or ferric chloride solution. Ferric chloride from electrolytic iron caused hemoglobin regeneration so that in 9 weeks a value of 16% was obtained. The electrolytic iron, FeCl3, and FeCl3solution were copper free as shown by the Hilger spectrograph. If CuSO4be given with the ferric chloride, regeneration is quicker and requires 4 weeks to reach a value of 2.2% higher than without copper.Rats in glass cages with glass screens did not become anemic any sooner than rats in cages with galvanized screens. Rats on shavings did not develop anemia in 20 weeks. Anemic rats were given sucrose dissolved in copper free water. One lot received in addition pure FeCl3, another lot received 3.0 mg. copper as CuSO4per rat daily, and the third lot received sucrose and distilled water. The FeCl3lot had a hemoglobin value of 15% in 3 weeks. The CuSO4lot showed a slight gain in hemoglobin, due to a small amount of iron in the c.p. CuSO4. The control lot showed no gain in hemoglobin, so after 2 weeks each rat was given daily 0.2 mg. of Fe as FeCl3; and in 2 weeks the hemoglobin increased from 5 to 12%.

To the Editor: In the article on poison ivy (Rhus) dermatitis, by A. M. Kligman (A. M. A. Arch. Dermat. 77:149 [Feb.] 1958), the last conclusion (p. 177) reads as follows: "The treatment of Rhus dermatitis by the administration of Rhus allergens during the acute attack is irrational and hazardous."This statement seems to be based mainly on the severe toxic effects encountered by Kligman, who gave intramuscular injections with enormous and heroic doses of 3-n-pentadecyl catechol (0.2 cc. of 10% solution or 20 mg.) to 11 patients having acute poison ivy dermatitis. Of these 11 patients, at least 2 had such severe reactions as to warrant hospitalization; the remainder had varying degrees of systemic and local reactions.These data do not show that it is hazardous or even irrational to administer Rhus allergens during an attack of poison ivy dermatitis unless high concentrations of the allergens are given. This