The functioning of the Cuban home hospitalization programme: a descriptive analysis

Background  

Over the last decades hospital at home (HaH) programmes have been set up in many, mainly European, countries. The Cuban HaH programme is not hospital driven, but the responsibility of the first line health services, and family doctors play a pivotal role.     

Pathogenesis of refractory secondary hyperparathyroidism

Calcitriol is currently used to reduce parathyroid hormone (PTH) levels in uremic patients. However, a significant number of patients fail to respond to calcitriol therapy. The data suggest that a poor response to calcitriol can be anticipated in patients with severe hyperparathyroidism (with a high basal PTH levels) and uncontrolled serum phosphate. The abnormal parathyroid response to calcitriol in uremic patients with severe parathyroid hyperplasia may be attributed, to a large extent, to the development of nodular hyperplasia as a result of clonal transformation from a diffuse polyclonal hyperplasia. The factors involved in the development of polyclonal parathyroid hyperplasia, at earlier stages of secondary hyperparathyroidism, appear to be the same factors that stimulate PTH secretion and synthesis: hypocalcemia, hyperphosphatemia and low serum calcitriol levels. Studies performed in vitro using parathyroid tissue from uremic patients who required parathyroidectomy demonstrate that in nodular hyperplasia there is an abnormal response to calcium and calcitriol, which suggests that there are factors intrinsic to the hyperplastic cell (such as decrease in calcium sensor receptors and vitamin D receptors) responsible for an abnormal regulation of parathyroid function. Accumulation of phosphate is a key factor in the pathogenesis of secondary hyperparathyroidism and a poor response to calcitriol treatment is associated with the failure to control the serum phosphorus. High phosphate stimulates PTH secretion as demonstrated by in vivo and in vitro studies. In addition, animal studies strongly suggest that phosphate increases parathyroid cell proliferation. There are growth-related genes potentially involved in uremic hyperparathyroidism; however, changes in the expression of these genes may be the consequence rather than the cause of parathyroid hyperplasia.     

Release of transforming growth factor beta-1 in a vestibular schwannoma cell line

Vestibular schwannoma (VS) often displays an irregular growth pattern due to factors which remain unknown. In this study, VS cell lines from tissue removed during surgery were cultured in order to assess the presence of transforming growth factor beta-1 (TGFbeta-1) a multifunctional polypeptide that has different pleiotropic effects on various tissues. The antibody-binding inhibition assay technique was used. The proliferation rate of VS cell lines in vitro was assessed by [3H]thymidine incorporation, with determinations carried out on days 0, 1, 2 and 4 after removal of fetal calf serum (FCS) from the medium. After 48 h of FCS deprivation, cell growth decreased. TGFbeta-1 release also decreased progressively 24 h after removing FCS from the medium, reaching an overall decrease of 50% after 3 days. The cell culturing procedure appeared suitable for VS cells, in that VS cultures were viable for at least 4 months. TGFbeta-1 was initially shown to be released in significant amounts, but also to decrease progressively to values five times lower after 4 days. These data thus support the possibility of a significant association between TGFbeta-1 release and VS cell replication.     

Quantitative real-time PCR based on single copy gene sequence for detection of Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis

OBJECTIVE: To establish a method for quantification of Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis from subgingival plaque by real-time polymerase chain reaction (PCR) technique. MATERIAL AND METHODS: Bacterial cells from both species were obtained from type culture and counted microscopically. Cellular suspension in sterile distilled water was used for DNA extraction by boiling for 20 min, with a mineral oil cover. Primers for PCR were selected from sequences of LktC gene (A. actinomycetemcomitans) and Arg-gingipain (P. gingivalis) to yield amplicons below 100 bp. SYBR Green I based real-time PCR was adjusted to quantify separately both species. RESULTS: A good sensitivity and specificity were obtained for both species, although the yield was better for A. actinomycetemcomitans. A good repeatability of cycle threshold (CT) was encountered, so coefficient of variation was below 6% at every initial copy number. CONCLUSION: A new method of quantification of A. actinomycetemcomitans and P. gingivalis based on SYBR Green real-time PCR is presented. Its good sensibility and repeatability will allow its application to analysis of subgingival plaque samples.     

Modulation by thyroid hormones of rat parotid amylase secretion stimulated by 5-hydroxytryptamine

The effects of 5-hydroxytryptamine (5-HT) upon amylase secretion by rat parotid glands were studied in three groups of animals: (a) intact control rats (euthyroid rats); (b) hypothyroid rats obtained by surgical thyroidectomy 2 wk before the experiments; and (c) hyperthyroid rats obtained by the administration of sodium l-triiodothyronine for 2 wk before the experiments. Hyperthyroid rats showed significantly higher baseline amylase release than control rats. When the glands were stimulated with 5-HT (30 micro m), amylase release was significantly lower in the hypothyroid group and higher in the hyperthyroid rats than in control group. Addition of cholinergic, adrenergic or substance P antagonists did not modify 5-HT-stimulated amylase activity. The effects of 5-HT were partly but significantly blocked by the addition of 10 micro m methysergide (HT1/2/7 receptor blocker) in the three groups of rats. In contrast, 10 micro m ketanserine (HT2A receptor blocker) partly blocked the response to 5-HT only in the hyperthyroid animals. It was concluded that 5-HT induces amylase secretion by rat parotid glands through specific serotoninergic receptors, and that thyroid status modulates the 5-HT effect.