Differential expression of somatostatin receptor subtypes in brain.

The tetradecapeptide somatostatin has been implicated as an important regulator of neuronal and neuroendocrine function in the CNS. The cellular actions of somatostatin are mediated by specific receptors. The genes encoding two different somatostatin receptors (SSTRs) have been isolated and characterized, and RNA blotting studies have shown that both SSTR1 and SSTR2 are expressed in the brain. In order to gain a better understanding of the functions of somatostatin in the CNS, the distribution of SSTR1 and SSTR2 mRNAs was determined using the technique of in situ hybridization. SSTR1 mRNA was present throughout the mouse brain, particularly in the supra- and infragranular layers of the cortex, the amygdala, hippocampus, bed nucleus of the stria terminalis, substantia innominata, hypothalamus, pretectum, substantia nigra, parabrachial nucleus, and nucleus of the solitary tract. SSTR2 mRNA was primarily observed in the infragranular layers of the cortex, the amygdala, claustrum, endopiriform nucleus, arcuate and paraventricular nuclei of the hypothalamus, and medial habenular nucleus. Several regions of the brain reported to contain dense somatostatin-like immunoreactive terminal fields and receptor binding sites were devoid of both SSTR1 and SSTR2 mRNA, suggesting the existence of additional SSTR subtypes.     

磁性明胶微球体内分布实验研究

对磁性明胶微球进行了同位素标记。用γ-闪烁照相技术观察了磁性明胶微球在兔体内的分布。结果表明:靶部位的放射活性加磁场是未加磁场的15倍,而且施加磁场时间长和磁场强度大有利于磁性明胶微球定位于靶区。文中也介绍了自行设计的外加磁场装置。     

Trabecular bone architecture in female renal allograft recipients-- assessed by computed tomography

BACKGROUND: Osteopenia with decreased bone mineral density (BMD) is a frequent finding in renal allograft recipients. Data concerning the bone architecture in these patients do not exist, however. METHODS: We compared the bone architecture of 33 randomly assigned women (age 49 +/- 12 years), who had received renal allografts 5.6 +/- 5.3 years before the investigation, with 74 women (age 50 +/- 14 years) who were admitted for osteodensitometry. All patients underwent single-energy computed tomography (SEQCT) and a midvertebral high-resolution tomography with computer-assisted analysis of the trabecular vertebral body architecture. RESULTS: Progressive alteration of bone architecture was associated with increasing vertebral height loss of the vertebral body. Height reduction of a vertebral body of more than 15% was associated with a significantly lower BMD (-2.3 +/- 0.8 versus -1.1 +/- 1.1 standard deviations below normal BMD), a lower trabecular bone area (13 +/- 8% versus 42 +/- 22%) and a lower trabecular diameter (1.4 +/- 0.5 mm versus 2.2 +/- 0.8 mm) compared to recipients without height reduction. In comparison to a matched group of patients with similarly reduced BMD (1.1 +/- 1.2 versus 1.2 +/- 1.1 SD below normal BMD), renal allograft recipients showed a lower number of trabecular plates (5.6 +/- 3.1 versus 7.0 +/- 3.7) and a smaller intertrabecular surface (54 +/- 116 mm versus 75 +/- 138 mm). CONCLUSIONS: Alterations of bone architecture in renal allograft recipients were associated with progressive vertebral height loss. Despite similar bone mineral density, differences of bone architecture could be observed between renal allograft recipients and patients with osteoporosis.      

Central thrombi in pulmonary arterial hypertension detected by MR imaging

Differentiation of thrombi from slow flow in the pulmonary arteries, sometimes observed in the presence of pulmonary arterial hypertension, can be equivocal. Magnetic resonance (MR) imaging was performed in a patient with chronic pulmonary thromboembolism and pulmonary arterial hypertension using an electrocardiographically gated technique that allowed visualization of the pulmonary arteries at the end of diastole and multiple times during systole. These images were compared with those of a patient with primary pulmonary hypertension and those of healthy subjects. Thrombi were discrete structures, seen throughout the cardiac cycle on both the first and second spin-echo images, and decreased in signal intensity on the second image. Slow flow increased in signal intensity and changed in structure during the cardiac cycle and was seen best on the second image. MR may play an important role in excluding large central thrombi as the cause of pulmonary arterial hypertension. It is a noninvasive method for defining pulmonary arterial wall thickness and for direct visualization of chronic pulmonary thrombus.     

Autonomic responses and efferent pathways from the insular cortex in the rat

The anatomical distribution of autonomic, particularly cardiovascular, responses originating in the insular cortex was examined by using systematic electrical microstimulation. The localization of these responses to cell bodies in the insular cortex was demonstrated by using microinjection of the excitatory amino acid, D,L-homocysteic acid. The efferents from the cardiovascular responsive sites were traced by iontophoretic injection of the anterograde axonal tracer Phaseoleus vulgaris leucoagglutinin (PHA-L). Two distinct patterns of cardiovascular response were elicited from the insular cortex: an increase in arterial pressure accompanied by tachycardia or a decrease in arterial pressure with bradycardia. The pressor responses were obtained by stimulation of the rostral half of the posterior insular cortex while depressor sites were located in the caudal part of the posterior insular area. Both types of site were primarily located in the dysgranular and agranular insular cortex. Gastric motility changes originated from a separate but adjacent region immediately rostral to the cardiovascular responsive sites in the anterior insular cortex. Tracing of efferents with PHA-L indicated a number of differences in connectivity between the pressor and depressor sites. Pressor sites had substantially more intense connections with other limbic regions including the infralimbic cortex, the amygdala, the bed nucleus of the stria terminalis and the medial dorsal and intralaminar nuclei of the thalamus. Alternatively, the depressor region of the insular cortex more heavily innervated sensory areas of the brain including layer I of the primary somatosensory cortex, a peripheral region of the sensory relay nuclei of the thalamus and the caudal spinal trigeminal nucleus. In addition, there were topographical differences in the projection to the lateral hypothalamic area, the primary site of autonomic outflow for these responses from the insular cortex. These differences in connectivity may provide the anatomic substrate for the specific cardiovascular responses and behaviors integrated in the insular cortex.     

Proliferation of human malignant hematopoietic cells in immunodeficient mice: suppression by antibody to pluripotent K-562 leukemia cells involves direct cytolysis and effector cells

Six human hematopoetic cell lines were successfully heterotransplanted into athymic (nude) and asplenic-athymic (lasat) neonatal mice. The tumors arising from leukemia and lymphoma cells could then be serially transplanted into adult nude mice. Seven days after the fourth serial mouse passage, each mouse was treated with goat immune gamma globulin against K-562 cells. One control group was treated similarly, but with nonimmune (normal) gamma globulin, while another control group was not treated. The goat gamma globulin was not toxic for nude and lasat mice, and the immune, but not the normal, gamma globulin suppressed local subcutaneous growth of myelosarcomas, lymphosarcomas, and Burkitt lymphoma cells. On the other hand, the growth of lung, breast, and prostatic carcinomas and a melanoma of human origin were not altered by the immune gamma globulin. Since suppression of cell growth occurred equally well in decomplemented mice, a complement-mediated cytotoxicity apparently cannot be considered as responsible for the abrogation. The Fab fragment of the immunoglobulin did not suppress the growth of the myelosarcomas. We conclude that antibody suppression of the in vivo proliferation was specific for malignant hematopoietic cells and that the Fc portion of IgG is necessary for in vivo cytolysis of leukemia cells. The most probable mechanisms are direct antibody cytolysis and antibody-dependent macrophage-mediated cytotoxicity.     

Expression of bcl-xL can confer a multidrug resistance phenotype

It has been suggested that genes that regulate apoptotic cell death may play an important role in determining the sensitivity of tumor cells to chemotherapy. We have recently cloned a member of the bcl-2 family, bcl- x. To test whether bcl-XL expression affects the sensitivity of tumor cells to chemotherapy, we have created stable cell lines overexpressing bcl-XL and have tested these cells for resistance to cell death induced by metabolic inhibitors and chemotherapeutic agents. Bcl-XL expression dramatically reduces the cytotoxicity of bleomycin, cisplatin, etoposide, vincristine, hygromycin B, and mycophenolic acid for up to 4 days in culture. Bcl-XL does not prevent cells from undergoing cell cycle arrest in response to these drugs, but rather prevents treated cells from undergoing apoptosis. Cell-cycle analysis on cells treated with the chemotherapeutic agents bleomycin, cisplatin, etoposide, and vincristine, show that the drugs cause growth arrest in different positions within the cell cycle. Bcl-XL expressing cells treated with chemotherapeutic drugs retain their proliferative ability after the drugs are removed. Interestingly, vincristine-treated cells expressing bcl-XL become polyploid after drug removal. These data show that bcl-XL protects cells from a wide variety of apoptotic stimuli, acts in multiple positions within the cell cycle, and confers a multidrug resistance phenotype. The ability of bcl-XL to prevent apoptotic cell death in response to chemotherapy-induced DNA damage and cell-cycle arrest may contribute to the accumulation of chromosomal aberrations within tumors. The expression of bcl-XL in tumor cells is likely to be an important indicator of chemotherapeutic efficacy.     

Characteristics of Yoga Users: Results of a National Survey

Background  There are limited data on the characteristics of yoga users in the U.S. Objective  To characterize yoga users, medical reasons for use, perceptions of helpfulness, and disclosure of use to medical professionals. Methods  Utilizing cross-sectional survey data from the 2002 National Health Interview Survey (NHIS) Alternative Medicine Supplement (n = 31044), we examined correlates of yoga use for health. The estimated prevalence from 2002 NHIS of yoga for health was 5.1% corresponding to over 10 million adults. Results  In 2002, yoga users were predominately Caucasian (85%) and female (76%) with a mean age of 39.5 years. Compared to non-yoga users, yoga users were more likely female (OR 3.76, 95% CI 3.11–4.33); less likely black than white (OR 0.65, 95% CI 0.53–0.80); tended to be younger; and more likely college educated (OR 2.70, 95% CI 2.37–3.08). Musculoskeletal conditions (OR 1.61, 95% CI 1.42–1.83), mental health conditions (OR 1.43, 95% CI 1.22–1.67), severe sprains in the last 12 months (OR 1.49, 95% CI 1.22–1.81), and asthma (OR 1.27, 95% CI 1.05–1.54) were independently associated with higher yoga use, while hypertension (OR 0.78, 95% CI 0.64–0.95) and chronic obstructive lung disease (OR 0.69, 95% CI 0.48–1.00) were associated with lower use. Yoga was most commonly used to treat musculoskeletal or mental health conditions, and most users reported yoga to be helpful for these conditions. A majority of yoga users (61%) felt yoga was important in maintaining health, though only 25% disclosed yoga practice to their medical professional. Conclusions  We found that yoga users are more likely to be white, female, young and college educated. Yoga users report benefit for musculoskeletal conditions and mental health, indicating that further research on the efficacy of yoga for the treatment and/or prevention of these conditions is warranted.