First Report of Copper-Tolerant Pseudomonas syringae pv. tomato in Virginia.

Bacterial speck of tomato, caused by Pseudomonas syringae pv. tomato, is an important disease of fresh-market tomatoes along the Eastern Shore of Virginia. P. syringae pv. tomato was first identified in Northampton County on 17 May 1993, using the Biolog software program. During the spring of 1998, a field of tomato plants showed symptoms of bacterial speck. Three isolations on tryptic soy agar were made from symptomatic leaves and fruit tissues taken from young transplanted tomato plants, cv. Sunpride. The isolates were identified as P. syringae pv. tomato, using Biolog. A representative isolate was sent to the Pennsylvania Department of Agriculture, Plant Disease Diagnostic Laboratory, Harrisburg, for confirmation. The Virginia isolate was transferred to King's medium B, and identification of P. syringae pv. tomato was confirmed by fulfilling Koch's postulates, matching with the Biolog database, and testing for levan production (+), oxidase reaction (-), potato soft rot (-), arginine dihydrolase production (-), and tobacco hypersensitivity (+). In vitro growth inhibition of the 1998 Virginia P. syringae pv. tomato isolate required anhydrous cupric sulfate at 368 µg/ml compared with only 175 µg/ml for a known copper-sensitive 1998 Pennsylvania isolate. Therefore, the 1998 Virginia isolate was considered a copper-tolerant strain of P. syringae pv. tomato. For field evaluation, three copper treatments and two noncopper treatments were established in a randomized complete block design replicated four times. Treatments were initiated on 19 May and reapplied every 7 days for a total of 10 applications. Three disease ratings were taken every 7 days beginning on 30 June. For copper hydroxide (2.24 kg/ha; Kocide DF) plus mancozeb (2.24 kg/ha; Dithane); chlorothalonil (2.34 liters/ha; Bravo) plus copper salts of fatty and rosin acids (2.34 liters/ha; Tenncop); 2% maneb plus 66% copper sulfate (6.72 kg/ha; Cuprofix); and an untreated control, area under the disease progress curve (AUDPC) values were 319, 468, 478, and 438, respectively. There was no significant difference (P = 0.05) between the copper treatments and untreated control, confirming laboratory findings. In contrast, noncopper treatments of acibenzolar (21g/ha; Actigard), and acibenzolar (21 g/ha) plus mancozeb (2.24 kg/ha) (Actigard plus Dithane) were significantly different (P = 0.05) from the untreated control and copper treatments with AUDPC values of 116 and 160, respectively. This is the first report of copper-tolerant P. syringae pv. tomato in Virginia.

[Intracytoplasmic injection (ICSI) of cryopreserved testicular spermatozoa (Cryo-TESE): a retrospective study of the first 250 treatment cycles]. / Intrazytoplasmatische Injektion (ICSI) von kryokonservierten testikulären Spermatozoen (Kryo-TESE): Eine retrospektive Analyse der ersten 250 Behandlungszyklen.

It is reported on the results of 250 treatment cycles in which we carried out intracytoplasmic injections (ICSI) with frozen and thawed testicular spermatozoa (cryo-TESE). Up to July 1997 we treated 127 patients, 225 embryo transfers were performed (90%), and an average of 2.3 preimplantation embryos were transferred. This resulted in 53 clinical pregnancies, six patients aborted (11.3%). The pregnancy rate was 21.2% per treatment cycle, 23.5% per embryo transfer, and 41.7% per patient. This so called cumulative pregnancy rate is still about to rise, because 49 out of the 72 non-pregnant patients are still in our ICSI-program. Twenty-two children are born, 2 twins and 1 triplet. All children are healthy and without any major malformations. We conclude from these results that using cryopreserved testicular sperm for ICSI is an effective and successful approach for the treatment of severe testicular insufficiency. In comparison to the use of native testicular sperm with the necessity of repetitive testicular biopsies, cryopreservation is advantageous in many concerns (e.g. logistic, organisatoric and financial) and is therefore recommended for clinical routine.

[Intracytoplasmic injection of epididymal and testicular sperm after failed heterologous insemination]. / Zur intrazytoplasmatischen Injektion von epididymalen und testikulären Spermien nach frustranen heterologen Inseminationen.

We report on our experiences with intracytoplasmic injection (ICSI) of epididymal and testicular spermatozoa (MESA, TESE) from azoospermic men whose wives had previously failed to become pregnant after several cycles of artificial insemination by donor (AID); because we do not perform AID treatment in our clinic, all these treatments were carried out in other fertility centers as well as the female diagnostic of sterility. In 3 husbands we could not find any testicular spermatozoa or spermatids, leaving 15 women under treatment. Of these 15 women, 9 became pregnant. This accounts for a pregnancy rate per patient of 60%. We believe that functional defects of the oocytes and somatizing psychological problems concerning AID are predominantly responsible for these results and that both problems can be overcome by ICSI. Besides, these results demonstrate that ICSI/MESA and ICSI/TESE are effective approaches in the treatment of azoospermic men and that using cryopreserved spermatozoa is not disadvantageous in the outcome of ICSI.

Epilepsy and fragile X gene mutations.

We used two strategies to investigate a possible link between predisposition for epilepsy and mutations in the fragile X mental retardation-1 gene. The first entailed performing electroencephalography on 14 patients with an amplification in the fragile X mental retardation-1 gene, and the second involved molecular genetic analysis of the fragile X mental retardation-1 gene in 16 children with benign childhood epilepsy with centrotemporal spikes (BECT, Rolandic epilepsy). Fourteen young male patients with fragile X syndrome, verified by a full mutation in exon 1 of the fragile X mental retardation-1 gene, were studied by electroencephalography. In eight boys aged between 4-8 years we observed focal sharp waves, activated by sleep. In six of these patients, partial seizures occurred during sleep. We detected no epileptiform electroencephalographic abnormalities under the age of 4 and over the age of 8. In 16 children with Rolandic epilepsy who were studied for fragile X gene mutations, one boy proved to carry a fragile X premutation. In the waking state electroencephalography of a 5-year-old girl with a premutation in one of her fragile X mental retardation-1 genes, we found groups of generalized spike wave complexes. Our observations suggest a possible impact of the fragile X mental retardation-1 gene mutations on brain maturation and epileptogenesis.

Prenatal diagnosis of the Pallister-Killian mosaic aneuploidy syndrome by CVS.

Prenatal cytogenetic analysis at 11 weeks of gestation revealed an abnormal karyotype 47,XX,+mar in all metaphases obtained from a chorionic villi sample after 24 h culture. Karyotyping of amniotic fluid cells in the second trimester showed mosaicism 47,XX,+i(12p)/46,XX with 10% aneuploid cells. The pregnancy was terminated at 20 weeks of gestation on the patient's request. The aborted fetus showed typical manifestations of the Pallister-Killian mosaic aneuploidy syndrome. The identity of the supernumerary isochromosome 12p was proven by LDH isozyme electrophoresis using cultured fibroblasts and by nonradioactive in situ hybridization using a biotinylated set of chromosome 12-specific DNA probes.

[The EEC-syndrome. Case report and some suggestions about its pathogenesis (author's transl)]. / Das EEC-Syndrom. Fallbericht und Uberlegungen zur Pathogenese.

The clinical data of a boy with ectrodactyly, ectodermal dysplasia, and cleft lip and palate (EEC-syndrome) are presented. Until now about 80 case histories with this syndrome have been published, 30 of them having all 3 symptoms. The combination of defects in rather different organs of ectodermal as well as mesodermal origin is difficult to understand. Changes in ectodermal tissues may well be the key factor in explaining the pathogenesis of this syndrome. This is supported by evidence gained by ontogenetical research with animals.

The Roberts' syndrome.

A report is given on a small-for-date male infant showing the following symptoms: bilateral aplasia of humerus, radius, and ulna, shortened femora, bilateral cleft lip and cleft palate, stigmata of dysmorphism, and notably; simple helix formation of the ear, simian crease, clinodactylia, bilateral clubfoot deformity, hypospadia, thrombocytopenia, micrognathia, and contractures in the knee joints. Postmortem autopsy revealed horsehoe kidney, ureterstenosis with hydronephrosis, persistent branchial arches, and absence of the knee joints. Chromosome analysis results performed by G-band technique turned out normal. This, obviously, was a case of the so-called Roberts' syndrome. Our results were compared with the relevant literature and some particularities were emphasized. The question was discussed as to whether the SC-phocomelia (pseudothalidomid syndrome), the TAR syndrome, and reported single cases might be an identical syndrome.

Asymmetrical, reciprocal translocation (45,XX,tdic(9;17) (p21;p12).

A nine-month-old girl with dysmorphic features, congenital heart disease and chromosomal mosaicism is reported. Approximately one-half of the cells (lymphocytes and fibroblasts) showed a normal karyotype 46, XX, the other half a dicentric translocation chromosome. Using the G-band technique, the dicentric chromosome was identified as a 9/17 translocation chromosome. Both centromeres of the translocation chromosome could be stained to the same degree, using the C-band technique. The centromere region of chromosome No. 9 was in addition demonstrated, by using the Giemsa 11 technique.

[A further example of chromosome 18q-associated with IgA deficiency in serum and saliva (author's transl)]. / Ein Beitrag zur 18q-Deletion mit Immungolbulinmangel

In a 3 1/2 years old boy with congenital malformations, statomotoric and mental retardation and immunological defects the chromosomal aberation 46,XY, 18q- was found. The result of the G-band analysis was 46,XY, del (18) (pter yields q11::q21 leads q ter) or 46,XY, del (18) (pter leads q21). The structural genes for the systems Gm, PGM-1 and HL-A presumably are not localized on the deleted chromosomal segment.