A combination of additive group contributions and nonadditive molecular parameters is employed to estimate the normal melting points of 1215 organic compounds. The melting points are calculated from the ratio of the total phase change enthalpy and entropy of melting. The total phase change enthalpy of melting is calculated from the enthalpic group contributions, whereas the total phase change entropy of melting is estimated using a semiempirical equation based on only two nonadditive molecular parameters. The average absolute error in estimating the melting points of these organic compounds is 33.2 K. This is a relatively low value considering the wide range of pharmaceutically and environmentally relevant organic compounds included in this data set.

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The aim of this study is to provide a simple means of estimating the total entropy of melting (∆S m tot ) for a wide range of pharmaceutically and environmentally relevant organic compounds. A semiempirical equation based on only 2 molecular descriptors, the rotational symmetry number(σ) and the molecular flexibility number (Φ), has been used to calculate ∆S m tot for 1799 organic compounds. The average absolute error in estimating ∆S m tot is 12.3 J/K‚mol. This method gives entropy predictions that are comparable to those of a recently published group additivity method that utilizes 144 group contribution values.

Changes of angiotensin II and cAMP in plasma, brain tissue, adrenal gland and cardiovascular tissue during the acute and chronic stress were studied in rats. The acute stress group was subjected to compulsive cold water swimming for 20min, while the chronic stress group was exposed to an ambient temperature of 4–8°C for 5 days. The results indicated that plasma angiotensin II levels were significantly increased in both stress groups, reaching up to 900% and 134% of the control in the acute and chronic groups, respectively. Angiotensin II contents in the anterior hypothalamus, medulla oblongata, myocardium, vasculature and adrenals were also elevated in both groups. With the exception of the adrenals, the contents of tissue angiotensin II in the chronic stress animals were significantly higher than those of the acute stress animals. In contrast, cAMP levels in plasma and tissue (hypothalamus and adrenals) and corticosterone levels in plasma in the acute stress group were all higher than those in the chronic stress animals, although the levels of the latter group were also increased compared with the control group. These results suggest that circulating and tissue angiotensin II may play an important role in the acute and chronic stress responses and that angiotensin II should be classified as a stress hormone.

Women with endometriosis (EMs) have unexplained infertility. The recently identified telocytes (TCs) might participate in the maintenance of structural and functional integrity of oviduct tissue, but so far the involvement of TCs in EMs-affected oviduct tissue and potential impact on fertility capacity remain unknown. By an integrated technique of haematoxylin and eosin staining, in situ immunohistochemistry and double-labelled immunofluorescence staining and electron microscopy approach, TCs were studied in the autotransplantation Sprague–Dawley rat model of EMs-affected oviduct tissue and in sham control, respectively, together with determination of iNOS, COX-2, LPO and estradiol. TCs were found in perivascular connective tissue and smooth muscle bundles in sham oviduct, with typical ultrastructural features (a slender piriform/spindle/triangular cell body, and one or more extremely long prolongations, emerged from cell bodies and extend to various directions), and specific immunophenotype of CD34-positive/vimentin-positive/c-kit-negative. However, in EMs-affected oviduct tissue (grade III), extensive ultrastructural damage (degeneration, discontinue, dissolution and destruction), significant decrease or loss of TCs and interstitial fibrosis were observed, together with elevated level of iNOS, COX-2, LPO and estradiol, thus suggestive of inflammation and ischaemia-induced TCs damage. Based on TCs distribution and intercellular connections, we proposed that such damage might be involved in structural and functional abnormalities of oviduct, such as attenuated intercellular signalling and oviduct contractility, impaired immunoregulation and stem cell-mediated tissue repair, 3-D interstitial architectural derangement and tissue fibrosis. Therefore, TCs damage might provide a new explanation and potential target for EMs-induced tubal damage and fertility disorders.