The crying infant and the family

Crying is one of the first forms of communication between the baby and his#shher family. The reaction of the family to baby's crying was studied during the first six months. Twenty-eight babies entered in the study. A questionnaire and personal visits were used. Ninety-six correlations were analysed by computer.

1. A certain amount of crying can be considered physiological which seems to be independent from external stimuli.
2. The crying of an infant seems to be greatly affected by the anxiety and the tense atmosphere of the family.
3. The so-called “good baby” is cuddled significantly less.
4. If the mother considered the crying to be a normal signal of a healthy baby, she usually used only one method to calm the infant.
5. The feeding behaviour of the infant did not seem to influence the mother's response to crying.
6. The dummy was the most commonly used method to quieten a baby.
7. When either one or more methods were used to soothe a baby, they were successful in 85 per cent of cases.
     

On the Formation Mechanism of Column Damage Within Modular Taper Junctions

BackgroundColumn damage is a unique degradation pattern observed in cobalt-chromium-molybdenum (CoCrMo) femoral head taper surfaces that resemble column-like troughs in the proximal-distal direction. We investigate the metallurgical origin of this phenomenon.MethodsThirty-two severely damaged CoCrMo femoral head retrievals from 7 different manufacturers were investigated for the presence of column damage and chemical inhomogeneities within the alloy microstructure via metallographic evaluation of samples sectioned off from the femoral heads.ResultsColumn damage was found to affect 37.5% of the CoCrMo femoral heads in this study. All the column-damaged femoral heads exhibited chemical inhomogeneities within their microstructures, which comprised of regions enriched or depleted in molybdenum and chromium. Column damage appears as a dissolution of the entire surface with preferential corrosion along the molybdenum and chromium depleted regions.ConclusionMolybdenum and chromium depleted zones serve as initiation sites for in vivo corrosion of the taper surface. Through crevice corrosion, the degradation spreads to the adjacent non-compositionally depleted areas of the alloy as well. Future improved alloy and processing recipes are required to ensure no chemical inhomogeneity due to segregation of solute elements are present in CoCrMo femoral heads.     

Diabetes-related intestinal region-specific thickening of ganglionic basement membrane and regionally decreased matrix metalloproteinase 9 expression in myenteric ganglia

BACKGROUNDThe importance of the neuronal microenvironment has been recently highlighted in gut region-specific diabetic enteric neuropathy. Regionally distinct thickening of endothelial basement membrane (BM) of intestinal capillaries supplying the myenteric ganglia coincide with neuronal damage in different intestinal segments. Accelerated synthesis of matrix molecules and reduced degradation of matrix components may also contribute to the imbalance of extracellular matrix dynamics resulting in BM thickening. Among the matrix degrading proteinases, matrix metalloproteinase 9 (MMP9) and its tissue inhibitor (TIMP1) are essential in regulating extracellular matrix remodelling.AIMTo evaluate the intestinal segment-specific effects of diabetes and insulin replacement on ganglionic BM thickness, MMP9 and TIMP1 expression.METHODSTen weeks after the onset of hyperglycaemia gut segments were taken from the duodenum and ileum of streptozotocin-induced diabetic, insulin-treated diabetic and sex- and age-matched control rats. The thickness of BM surrounding myenteric ganglia was measured by electron microscopic morphometry. Whole-mount preparations of myenteric plexus were prepared from the different gut regions for MMP9/TIMP1 double-labelling fluorescent immunohistochemistry. Post-embedding immunogold electron microscopy was applied on ultrathin sections to evaluate the MMP9 and TIMP1 expression in myenteric ganglia and their microenvironment from different gut segments and conditions. The MMP9 and TIMP1 messenger ribonucleic acid (mRNA) level was measured by quantitative polymerase chain reaction.RESULTSTen weeks after the onset of hyperglycaemia, the ganglionic BM was significantly thickened in the diabetic ileum, while it remained intact in the duodenum. The immediate insulin treatment prevented the diabetes-related thickening of the BM surrounding the ileal myenteric ganglia. Quantification of particle density showed an increasing tendency for MMP9 and a decreasing tendency for TIMP1 from the proximal to the distal small intestine under control conditions. In the diabetic ileum, the number of MMP9-indicating gold particles decreased in myenteric ganglia, endothelial cells of capillaries and intestinal smooth muscle cells, however, it remained unchanged in all duodenal compartments. The MMP9/TIMP1 ratio was also decreased in ileal ganglia only. However, a marked segment-specific induction was revealed in MMP9 and TIMP1 at the mRNA levels.CONCLUSIONThese findings support that the regional decrease in MMP9 expression in myenteric ganglia and their microenvironment may contribute to extracellular matrix accumulation, resulting in a region-specific thickening of ganglionic BM.     

Inhibition by interleukin-1\ of noradrenaline release in rat spleen: involvement of lymphocytes,NO and opioid receptors

Effects of indomethacin, N-nitro-L-arginine (NNA) and naloxone, and of pretreatment with cyclophosphamide (CY), on the interleukin (IL)-I\ induced inhibition of exocytotic noradrenaline release were investigated in the isolated, vascularly perfused spleen of the rat. Neurotransmitter release was evoked by perivascular electrical stimulation (4 Hz) and the overflow of endogenous noradrenaline was determined by HPLC with electrochemical detection.Perfusion of the spleen with Tyrode's solution containing IL-1\ (100 pg/ml) for 90 min caused an inhibition of the stimulation-evoked noradrenaline overflow which persisted for at least 20 min after washout of the IL. The evoked overflow was reduced in the presence of NNA 30 mol/l, but remained unaffected by indomethacin 3 mol/l, naloxone 0.1 mol/l or treatment of the rats with CY (250 mg/kg). The opioid agonist etorphine 10 mol/1 inhibited the evoked overflow of noradrenaline and this effect was prevented by naloxone 0.1 mol/1. The inhibition of evoked overflow by IL-1\ was not affected by indomethacin but was reduced or even prevented in the presence of NNA or naloxone, or after lymphocyte depletion of spleens by CY.The results are compatible with the idea that in the rat spleen exocytotic noradrenaline release is accompanied by a concomitant secretion of a nitric oxide (NO)-like compound which, in turn, reinforces noradrenaline release, and that the release can be inhibited via prejunctional opioid receptors. The IL-1\ induced inhibition of evoked release appears to be a complex process which involves as one of many steps a decrease of the facilitatory NO-like compound and the release of endogenous opioids probably from spleen lymphocytes.     

Studies on the interactions between C-reactive protein and complement proteins

Several studies have investigated the interactions between C-reactive protein (CRP) and various complement proteins but none of them took into consideration the different structural forms of CRP. The aim of our study was to investigate whether the different antigenic forms of CRP are able to bind C1q, to trigger activation of the C1 complex and to study the ability of the various CRP forms to bind complement factor H (FH) and C4b-binding protein (C4BP). Interactions between various CRP forms and complement proteins were analysed in enzyme-linked immunosorbent assay and surface plasmon resonance tests and activation of the C1 complex was followed in a reconstituted system using purified C1q, C1r and C1s in the presence of C1-INH. Native, ligand-unbound CRP activated the classical pathway weakly. After binding to phosphocholine, native CRP bound C1q and significantly activated C1. Native CRP complexed to phosphocholine did not bind the complement regulatory proteins FH and C4BP. After disruption of the pentameric structure of CRP, as achieved by urea-treatment or by site-directed mutagenesis, C1q binding and C1 activation further increased and the ability of CRP to bind complement regulatory proteins was revealed. C1q binds to CRP through its globular head domain. The binding sites on CRP for FH and C4BP seemed to be different from that of C1q. In conclusion, in parallel with the increase in the C1-activating ability of different CRP structural variants, the affinity for complement regulatory proteins also increased, providing the biological basis for limitation of excess complement activation.     

Maternal hyperandrogenism beginning from early pregnancy and progressing until delivery does not produce virilization of a female newborn

A 33-year-old primagravida with a history of polycystic ovary syndrome was referred because of symptoms of moderate hyperandrogenism. Serum hormone levels, measured regularly from the 7th week of pregnancy until delivery, showed very high increases of testosterone, androstenedione and estradiol. Ultrasound showed no evidence of adrenal or ovarian masses. She delivered a female newborn with normal female external genitalia. Umbilical cord hormone levels were normal, except for a modest increase of serum testosterone. After delivery the androgen levels of the mother returned to normal and the symptoms of hyperandrogenism were also slightly improved.