The symptomatology of the climacteric in relation to hormonal and cytological factors

Summary. Climacteric symptomatology was investigated in a group of non-selected women aged between 54 and 56 years of age, Vasomotor complaints and dyspareunia, in particular, were noted and related to plasma hormone levels and vaginal cytology. Only 33% of those women who were within 5 years of the menopause had symptoms of a magnitude that might require hormone replacement therapy. Neither the vasomotor complaints nor dyspareunia correlated with the hormone levels or cytology findings to such an extent as to be helpful in planning treatment. Aarently only a minority of women in their middle 50s demonstrate a symptomatic need for hormone replacement therapy and laboratory investigations are of little use in their identification.     

FOLLOW-UP TO 16 YEARS OF SCHOOL CHILDREN WHO HAD MARKED SPEECH DEFECTS AT 7 YEARS

Summary In this paper we present the results of a follow-up study to age 16 years of 215 children in the National Child Development Study who were reported to show marked speech defects with normal hearing at 7 years. At 16 years information was available for 180 (85%) of the surviving 212 children. 30% of these children were in special schools and of the 70% in ordinary schools, 51% were reported still to have a residual speech problem. Additional health and social problems were frequent among the study group children and with very few exceptions they did badly at school. The findings at 16 years strongly reinforce our earlier conclusions that markedly defective speech at 7 years indicates the likelihood of continued backwardness in the development of acceptable verbal communication, social maturity and scholastic attainments.     

Facilitatory effect of nicotine on adrenergic neuroeffector transmission in the isolated ear artery of the rabbit

The effects of nicotine were studied on perfusion pressure and vasoconstrictor responses to sympathetic nerve stimulation in the isolated ear artery of the rabbit. Infusions of nicotine (50 μM) produced a transient increase in perfusion pressure and potentiated responses to nerve stimulation; these effects of nicotine were unaffected by atropine (0–3 μM) and abolished or significantly reduced respectively by hexamethonium (300 μM) or mecamylamine (1 μM). In experiments with ear arteries previously labelled with [³ H] noradrenaline an infusion of nicotine (50 μM) produced a transient increase in tritium efflux and the potentiation of responses to nerve stimulation in the presence of nicotine was accompanied by a statistically significant increase in stimulation-induced tritium efflux; these effects of nicotine were abolished by hexamethonium (300 μM) or mecamylamine (1 μM).     

Transformation of slow- or fast-twitch rabbit muscles after cross-reinne rvation or low frequency stimulation does not alter the in vitro properties of their satellite cells

We previously showed that satellite cells isolated from rabbit fast-twitch and slow-twitch muscles presented different behaviours in culture; cells from slow muscle differentiated more quickly and fused into more numerous myotubes than those from fast muscle. Moreover, only slow-muscle derived satellite cells expressed in vitro the slow type I myosin heavy chain isoform (MyHC). We wanted to investigate whether the properties of satellite cells originating from different muscles were under the influence of the adult fibre type on which they were located. For this purpose, we transformed the properties of the adult rabbit fast-twitch semimembranosus accessorius (SMa; ∼100% type II fibres) and the slow-twitch semimembranosus proprius (SMp; 100% type I fibre) muscles by (1) cross-reinnervating the SMp with the main branch of the fast SMa nerve; or (2) electrical stimulation at 10 Hz of the SMa muscle. We studied their satellite cells in vitro. Five-month cross-reinnervation of the SMp induced a large shift of its MyHC type characteristics towards those of a fast muscle, and three-month electrical stimulation at low frequency transformed the fast-twitch SMa into a slow-twitch muscle, as shown by SDS--PAGE of MyHC. In spite of the transformation of their muscle characteristics, satellite cells in culture kept their original properties. Indeed, as shown by MyoD and myogenin gene expression as markers of fusion, satellite cells isolated from cross-reinnervated and from control SMp began to fuse by eight days of culture, and expressed MyoD and myogenin at that stage. Later they differentiated into numerous myotubes. Satellite cells isolated from electrically stimulated and control SMa presented a similar behaviour in culture: they did not express MyoD and myogenin at eight days, and fused by ten days into only a few myotubes. Moreover, MyHC gene expression showed that, in contrast with slow-muscle derived satellite cells, the type I MyHC gene was not expressed by satellite cells isolated from the stimulated SMa in spite of its homogeneous type I fibre composition. Taken together, these data support the idea that once constituted, muscle fibre types per se do not influence the properties of their associated satellite cellsThis revised version was published online in July 2005 with corrections to the Cover Date.     

Molecular detection of t(8;21)/AML1-ETO in AML M1/M2: correlation with cytogenetics, morphology and immunophenotype

The t(8;21) identifies a subgroup of acute myeloid leukaemia (AML) with a relatively good prognosis which may merit different treatment. It is associated predominantly, but not exclusively, with AML M2, and corresponds to rearrangements involving the AML1 and ETO genes. AML1-ETO positive, t(8;21) negative cases are well recognized but their incidence is unknown. In order to determine optimal prospective AML1-ETO RT-PCR screening strategies, we analysed 64 unselected AML M1 and M2 cases and correlated the results with other biological parameters. Molecular screening increased the overall detection rate from 8% to 14%. AML1-ETO was found in 3% (1/32) of AML M1 and 25% (8/32) of M2, including three patients without a classic t(8;21) but with chromosome 8 abnormalities. It was more common in younger patients. Correlation with morphology enabled development of a scoring system which detected all nine AML1-ETO-positive cases with a false positive rate of 7% (4/55). Although certain AML1-ETO-positive cases demonstrated characteristic immunological features (CD19 and CD34 expression, CD33 negativity), each of these markers was insufficiently specific to permit prediction in an individual case. We conclude that initial routine prospective molecular screening for AML1-ETO in all AMLs, combined with standardized morphological and immunological analysis, is desirable in order to produce improved prognostic stratification and to determine whether screening can ultimately be restricted to appropriate subgroups.     

Protection by Zinc-Metallothionein (ZnMT) against Cadmium-Metallothionein-Induced Nephrotoxicity

In contrast to inorganic Cd, acute iv administration of Cd boundto metallothionein (CdMT) concentrates in renal tissue. Thisuptake of CdMT produces functional and morphological changesin kidneys, similar to those observed after chronic exposureto inorganic Cd. In order to examine the importance of the metalcomponent of MT in the renal uptake of MT, the renal concentrationof ³⁵S after administration of [³⁵S]ZnMT and [³⁵S]CdMT was compared.Renal uptake of ³⁵S from both CdMT and ZnMT was very rapid,with peak concentrations observed 15–30 min after administration.³⁵S in kidneys increased in a dose-dependent manner after administrationof various doses of [³⁵S]ZnMT, up to 1.3 µmole MT/kg;however, higher doses did not further increase renal ³⁵S concentrations.A similar saturation of ³⁵S reabsorption was observed for therenal uptake of [³⁵S]CdMT. CdMT produced renal injury with dosesas low as 0.26 µmol MT/kg (0.2 mg Cd/kg). In contrast,with a dose of ZnMT as high as 5.12 µmol MT/kg (2 mg Zn/kg),no histopathological changes were observed. Therefore, ZnMTappears to be nontoxic even though ZnMT delivers more MT tothe kidney than does CdMT. Because ZnMT and CdMT are apparentlyhandled by the same renal transport mechanism, the effects ofZnMT on ¹⁰⁹CdMT renal uptake and nephrotoxicity were determined.One group of mice was given a nephrotoxic dose of ¹⁰⁹CdMT (0.51µmol MT/kg containing 0.4 mg Cd/kg, iv), and the othergroup received an equimolar dose of unlabeled ZnMT 1 min before¹⁰⁹CdMT administration. Renal function was evaluated by measuringurinary glucose and protein excretion, as well as histopathology.Marked renal toxicity was observed 24 hr after ¹⁰⁹CdMT administration.In contrast, renal function appeared normal in mice receivingZnMT before ¹⁰⁹CdMT. However, a similar concentration of ¹⁰⁹Cdwas found in kidneys of both groups. The present results demonstratethat ZnMT is not only nontoxic to the kidney at a dose as highas 5 µmol MT/kg, but can also protect against the nephrotoxiceffect of CdMT without decreasing renal Cd concentration.     

Coping Strategies of Infertile Women

This study was initiated to explore the coping patterns of infertile women. The researchers interviewed 30 women and evaluated data using content analysis. Six ways of coping with infertility were identified: (1) increasing the space or distancing oneself from reminders of infertility, (2) instituting measures for regaining control, (3) acting to increase self-esteem by being the best, (4) looking for hidden meaning in infertility, (5) giving in to feelings, and (6) sharing the burden with others.     

MORPHEA WITH HIGH TITER OF FIBRONECTIN ANTIBODIES

A 20-year-old man with a 9-year history of unusual subcutaneous morphea with nodular lesions in a circular arrangement and wooden-hard symmetrical induration of the arms, had high titers of fibronectin antibodies. A possible role of fibronectin and antifibronectin antibodies in the pathogenesis of scleroderma is discussed.     

Nursing Management of Mastitis Due to Breastfeeding

Mastitis secondary to breastfeeding is a very preventable condition in which the nurse can play a large role. The physiology of normal breastfeeding and the pathophysiology of mastitis are presented, along with nursing interventions and techniques with scientific rationale to prevent and treat mastitis.