Structural pluralism and all-cause mortality

OBJECTIVES: This study tested the hypothesis that "structural pluralism" reduces age-standardized mortality rates. Structural pluralism is defined as the potential for political competition in communities. METHODS: US counties were the units of analysis. Multiple regression techniques were used to test the hypothesis. RESULTS: Structural pluralism is a stronger determinant of lower mortality than any of the other variables examined--specifically, income, education, and medical facilities. CONCLUSIONS: These findings support the case for a new structural variable, pluralism, as a possible cause of lower mortality, and they indirectly support the significance of comparable ecologic dimensions, such as social trust.     

Effects of calcium channel modulators on the proliferation of mouse spleen lymphocytesin vitro

The effects of nimodipine (voltage-dependent calcium channel blocker), CGP 28392 and BAY K 8644 (novel dihydropyridine derivatives that are considered as calcium entry stimulators) on the spontaneous proliferation of mouse spleen lymphocytes were studiedin vitro. [³H]-thymidine incorporation into DNA of lymphocytes was used as an sensitive index of the cell proliferation. It has been found that nimodipine (10^–4 M–10^–6 M) significantly inhibited the [³H]-thymidine uptake in a dose dependent fashion with ED₅₀ value of 2.4×10^–5 M. Unexpectedly, CGP 28392 (10^–4 M–10^–7 M) acts as a calcium entry blocker and produces a strong inhibitory effect on lymphocyte proliferation (ED₅₀–2×10^–5 M). BAY K 8644 at a high concentration (10^–4 M) also has an inhibitory effect but at a lower concentration (10^–6 M–10^–10 M) significantly increased [³H]-thymidine uptake and abolished the inhibitory effect of nimodipine. This effect of nimodipine was also reversed by 5×10^–3 M calcium chloride. These findings indicate that calcium channel modulators can regulate the proliferation of mouse spleen lymphocytesin vitro.     

Effect of thymosin alpha 1 on hypothalamic hormone release.

Thymosin alpha 1 (T alpha 1) is a well-characterized immunopotentiating polypeptide originally isolated from calf thymus. We have recently shown in vivo, probable hypothalamic effects of T alpha 1 to decrease the release of the pituitary hormones, TSH, PRL and ACTH from the pituitary gland. Therefore, in the present study we evaluated the effect of the peptide on the release of hypothalamic regulatory hormones: thyrotropin-releasing hormone (TRH) and corticotropin-releasing hormone (CRH), as well as somatostatin (SRIH), from medial basal hypothalamic (MBH) fragments incubated in vitro. After a preliminary time-course study indicated that a 30-min incubation period was optimal, it was used for all the other experiments. At the end of the incubation the tissue was still able to respond to a depolarizing K+ concentration for 15 min by a 4-fold increase of TRH concentration compared to control basal release during the preceding 30 min. T alpha 1 was shown to inhibit the release of TRH and CRH from MBH fragments incubated in vitro with a minimal effective dose (MED) of 10(-11) M. SRIH and CRH release was also inhibited but the MED for these peptides was 10(-9) M. The relative responsiveness to the action of T alpha 1 was TRH greater than CRH, which was greater than SRIH. This correlated with our previous in vivo results for pituitary hormone release, except in the case of SRIH since we previously did not detect any significant effect of the peptide on growth hormone release. Finally, we evaluated the possible involvement of other neurotransmitters in the effect of T alpha 1 on TRH release.(ABSTRACT TRUNCATED AT 250 WORDS)