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S Yarkoni

Publications and source records attributed to S Yarkoni.

65 records · Page 4Linked to original sources
PubMed1978

Failure of bromocriptine to suppress prolactin in majeptil-induced hyperprolactinemia.

A case of hyperprolactinemic anovulation with amenorrhea and galactorrhea, due to Phenothizine derivative (Majeptil) is presented. Treatment with bromocriptine, 2.5 mg b.i.d., p.o., or L-Dopa, 500 mg, p.o., did not suppress serum prolactin and menstrual cycle was not resumed. Pituitary prolactin response to TRH and Pituitary LH and FSH response to LHRH were found to be normal. It seems that at the dose used, bromocriptine (a dopaminergic agonist) cannot counteract the phenothiazine induced hyperprolactinemia. Hence, it is not effective in induction of ovulation while the patient is under phenothiazine treatment.

Adult↗
PubMed1978

Experience with the Ypsilon (Soichet) intrauterine device.

The Ypsilon intrauterine device (IUD), which consists of stainless steel covered with silicone rubber, was studied in 209 women. In the 3,169 woman-months of use, there were 21 pregnancies, nine expulsions, and in 24 instances the Ypsilon IUD was removed for medical reasons (side effects). The net cumulative pregnancy rate in the 12 months after insertion was 6.4% and the expulsion rate was 3.8%; the medical removal rate was 9.0%. No perforations or tubal pregnancies occurred. The comparatively low medical removal rate renders the Ypsilon IUD a fairly good device for clinical use, although the pregnancy rate is rather high.

Adult↗
PubMed1976

Inversion homozygosity of chromosome no. 9 in a higly inbred kindred.

A pericentric inversion of chromosome no. 9 was present in seven of 10 members of a highly inbred kindred investigated; two were inversion homozygotes and five were heterozygotes. Inversion homozygosity was observed in both the propositus, ascertained because of ambiguous genitalia, and his phenotypically normal father. A phenotypically normal sister and brother with similar clinical findings proved to be inversion heterozygotes. These findings conclude that no causal relationship exists between the inversion and the abnormal phenotype.

Adult↗
PubMedDate not supplied

Can infantile hereditary agranulocytosis be diagnosed prenatally?

Fetoscopy and fetal blood sampling were performed in an attempt at prenatal monitoring of a pregnancy at risk for infantile hereditary agranulocytosis (Kostmann's disease). In smears of fetal blood three segmented neutrophils were found out of 200 nucleated cells (1 1/2 per cent). Their presence, although in a lower percentage than in six age-matched controls, was considered to indicate that the fetus was not affected. The newborn infant has developed normally and at the age of four months has a normal number of segmented neutrophils in his peripheral blood. Feasibility of prenatal diagnosis of infantile hereditary agranulocytosis is discussed.

Adult↗
PubMedDate not supplied

Incidence of BRCA1 and BRCA2 mutations in Ashkenazi colorectal cancer patients: preliminary study.

BACKGROUND: Mutations in BRCA genes are associated with an elevated incidence of colorectal cancer (CRC). While 20% of CRC patients have a familial history of colonic malignancies, in only 5% is the genetic setting understood. Thus, a majority of these patients lack any known genetic marker. Our aim was to explore the relevance of BRCA mutations to serve as such markers in the genetic screening and counseling of CRC patients. PATIENTS AND METHODS: 136 consecutive Israeli Jewish patients with sporadic CRC were screened for BRCA "Ashkenazi mutations": 185delAG, 5382insC and 6174delT. Carrier status was evaluated employing PCR, restriction analysis, SSCP and a Pronto BRCA kit. RESULTS: We found one 185delAG and two 6174delT carriers, altogether three Ashkenazi carriers out of 87 Ashkenazi patients tested, 3.5%. No carriers were found among the Arabs and non-Ashkenazi Jews surveyed. CONCLUSIONS: Our preliminary results show elevated rates of BRCA "Ashkenazi mutations" in Ashkenazi CRC patients, suggesting their involvement in CRC carcinogenesis. An implementation of a wider study will establish the role of these mutations as genetic markers for CRC.

Arabs↗