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Biomedical subjects

P Pakarinen

Publications and source records attributed to P Pakarinen.

44 records · Page 3Linked to original sources

Maternal serum copper and zinc concentrations in normal and small-for-date pregnancies.

Serum concentrations of copper (Cu) and zinc (Zn) were determined in 20 non-pregnant healthy menstruating women and in 20 pregnant women during the 1st, 2nd and 3rd trimesters and 5 weeks postpartum as a longitudinal study. Also a cross-sectional population of 106 women was studied. Further, Cu and Zn concentrations were measured in 13 pregnant women who gave birth to small-for-date (SFD) infants; this was done during the 3rd trimester of pregnancy. The serum Cu concentration in nonpregnant women was 0.91 +/- 0.19 mg/l. During pregnancy it was significantly higher (1.48 +/- 0.31, 1.91 +/- 0.25 and 2.20 +/- 0.36 mg/l during the 1st, 2nd and 3rd trimesters, respectively) and 5 weeks postpartum it was still higher (1.09 +/- 0.17 mg/l) than in the nonpregnant women. In the cross-sectional population, serum Cu and Zn values were of the same magnitude as in the longitudinal study. When longitudinal and cross-sectional values of serum Cu during the 3rd trimester were combined, the mean level (2.23 +/- 0.40 mg/l) was significantly higher than that in the SFD group (2.06 +/- 0.25 mg/l). Serum Zn in the SFD group (0.48 +/- 0.12 mg/l) did not differ significantly from the normal pregnant values.

Copper↗

The role of calcium, copper, iron and zinc in preterm delivery and premature rupture of fetal membranes.

Maternal and cord blood samples were collected in 60 cases with or without rupture of membranes before and at term. Serum concentrations of calcium, copper, iron and zinc were determined by proton-induced X-ray emission. Maternal and cord serum ceruloplasmin and maternal hemoglobin were also determined. Mothers with preterm delivery showed significantly lower hemoglobin values than those with delivery at term. Concentrations of calcium, iron and zinc were higher in cord than in maternal serum whereas maternal copper levels were higher than respective cord levels in all groups. The cord copper and ceruloplasmin and also their fetal/maternal ratios were significantly lower in the group with preterm premature rupture of fetal membranes (PROM) than in other groups. Maternal serum zinc and calcium were lower in preterm groups than in term groups. The study suggests a possible role of copper in preterm PROM and of zinc in the initiation of preterm labor, whereas calcium and iron do not seem to be involved in the etiology of prematurity or PROM.

Calcium↗

Copper and zinc in pre-eclampsia.

Twenty uncomplicated pregnancies, 10 parturients with mild and 10 parturients with severe pre-eclampsia, all with uncomplicated deliveries, were studied. Maternal and umbilical cord serum were checked for copper and zinc by the proton-induced X-ray emission (PIXE) method; maternal serum protein, hemoglobin and estriol were determined as well. Maternal zinc and copper values were lower, whereas the umbilical cord serum copper level was higher in the group with severe pre-eclampsia as compared with the controls. Maternal zinc was also lower in mild pre-eclampsia than in the controls. The possible causes of these changes are discussed in view of the hormonal, metabolic and enzymatic changes in pre-eclampsia.

Copper↗

Follicle-stimulating hormone ligand and receptor mutations, and gonadal dysfunction.

In contrast to the general contention, infertility can be an inherited condition. Some of the genetic causes of male and female infertility have turned out to be due to inactivating mutations in the gonadotropin and gonadotropin receptor genes. The topic of the present text is to review current knowledge on mutations affecting the function of follicle-stimulating hormone (FSH). This gonadotropin, by binding to its specific G protein-coupled cell membrane receptor (FSHR), is important for normal gonadal function. Mutations affecting gonadotropin genes are extremely rare, but recent genetic studies have revealed that the pathogenesis of subfertility or infertility can be due to mutations in the FSH receptor (FSHR) gene. While mutations affecting FSHR are sporadic, polymorphism of the FSHR gene seems to be a common phenomenon. To date, six inactivating and only one activating mutation have been detected in the FSHR gene. In contrast to LHR gene, the majority of these mutations affect the extracellular domain of the receptor. Together with animal models using the transgenic and knock-out approaches, systematic analysis of alterations in the FSHR gene increases our knowledge on the structure and function of the FSHR and demonstrates that the integrity of each FSHR segment is required for proper expression of the fully active protein and for normal gonadal function. Mutations in the FSHR gene have different consequences in the reproductive function depending on the sex of the patient: while normal ovarian function is critically dependent on FSH, male fertility is possible with minimal or absent FSH action.

Amino Acid Sequence↗

Characterization and developmental expression of a testis-specific adenosine deaminase mRNA in the mouse.

Adenosine is able to alter intracellular cAMP levels and to affect the physiological functions of sperm. It also modulates FSH action through its Gi protein coupled receptors. Adenosine deaminase (ADA), an enzyme regulating adenosine levels, exists in the plasma membrane of the sperm, but little is known about its action on testicular function. The present study investigates the expression of a testis-specific ADA mRNA with development and in comparison to several other tissues in the mouse. In addition, the sequence of a testis-specific ADA cDNA was determined from an adult mouse testis library. We demonstrate for the first time the presence of a major 1,350 bp testis-specific ADA mRNA and a weaker 1,200 bp ADA transcript whose developmental expression starts on day 28 of life. Sequence analysis of the testis-specific ADA cDNA indicated that exons 1 and 2, as well as the first 8 nucleotides of exon 3 of the somatic cell ADA cDNA were absent in the testicular ADA cDNA. The deduced open reading frame of the testis-specific ADA cDNA indicates absence of the first 51 amino acids at the 5' end that are present in the somatic cell ADA protein. The developmental onset of expression of the testis-specific ADA mRNA may be related to specific proliferation/differentiation events of spermatogenesis.

Adenosine Deaminase↗