The projection to the mesencephalon from the sensory trigeminal nuclei. An anatomical study in the cat

The terminal areas and the cells of origin of the projection from the sensory trigeminal nuclei to the mesencephalon were investigated, using the method of anterograde and retrograde transport of horseradish peroxidase or wheat germ agglutinin-horseradish peroxidase conjugate. Injection of tracer into the nucleus interpolaris or nucleus oralis (in the latter cases with involvement of the nucleus principalis) resulted in dense anterograde labeling in the deep and intermediate gray layers of the contralateral superior colliculus, extending throughout the rostrocaudal extent of the colliculus with the exception of its caudalmost part, which was not labeled. Minor projections to the intercollicular nucleus, posterior pretectal nucleus and nucleus of Darkschewitsch were found. Injection of tracer into the nucleus caudalis yielded a completely different result; terminal labeling in the midbrain was now present only in the periaqueductal gray matter, in its rostral and middle parts. The retrograde labeling observed after injection of tracer into the midbrain terminal areas showed that the cells of origin were located mainly in the alaminar spinal trigeminal nucleus, and the highest density of labeled neurons was found in the rostral part (subnucleus y) of the nucleus oralis. The retrograde labeling in the nucleus principalis was very sparse and almost exclusively involved peripherally located neurons. In the nucleus caudalis the overwhelming majority of the retrogradely labeled neurons were situated in its marginal layer. The functional implications of the above observations are discussed in relation to the findings in previous studies of the projections from the dorsal column nuclei and spinal cord to the midbrain. The combined results suggest that the trigeminal projections to the superior colliculus may be involved in the mechanisms of orientational behavior. The observation that the projection to the periaqueductal gray matter originates in the marginal layer suggests that it transmits information related to noxious stimuli.     

The role of microtubules in axoplasmic transport in vivo

To verify whether microtubules are involved in the mechanism of axoplasmic transport in vivo, [3H]leucine was injected into ventral horns of rats, and 3 h later Ca2+ or other drugs injected into sciatic nerves. The injection of 50-200 mM Ca2+, raising intra-axoplasmic Ca2+ levels, blocked transport above the intraneural injecting site and decreased microtubular density. Conversely, injection of 10 mM EGTA lowering the intra-axoplasmic Ca2+ induced the same changes. By combining the injection of 50 mM colchicine with 25 mM Ca2+ or 5 mM EGTA, the effects were additive in that transport was weakened further or even blocked and microtubules disappeared. Therefore, microtubules seemed to be a mediator between the injected drug and the blockade of transport and Ca2+ to be a regulator of axoplasmic transport in vivo. Tubulin, a subunit of microtubules, contains SH groups and Cd2+ is a chelate of them. By injection of 50-100 mM Cd2+, transport was weakened or blocked. The sulfhydryl inhibitor, N-ethylmaleimide increased, but the sulfhydryl donor, dimercaptosuccinate, abolished the effect of Cd2+ on transport. N-ethylmaleimide also amplified the Cd2+ effect on decreasing SH group content of sciatic nerve homogenate. There were 8.7 SH groups per tubulin monomer isolated from rabbit brain. The SH groups of tubulin in vitro and microtubular density in vivo were decreased with the increase of Cd2+ concentration. All these results indicated that microtubules play a role in the mechanism of axoplasmic transport.     

Adaptation to stress exposure prevents arrhythmogenic and contractural effects of the excess of Ca2+ on the heart by the increased activity of sarcoplasmic reticulum

Summary Adaptation of rats to repcated short-term stress exposure prevents, to a considerable extent, contractural and arrhythmogenic effects of high concentrations of extracellular Ca²⁺ on isolated heart. Increased efficiency of SR Ca²⁺-pump functioning and a significant increase in Ca²⁺ pump resistance to autolysis are proved to play the main role in this effect.     

增加腹部活动对腹膜透析小分子溶质转运的影响

目的 :探讨腹部震荡和摇摆是否能增加小分子溶质转运和膜腹透析的效能。方法 :采用自身前后对照 ,观察了 18例连续不卧床腹膜透析 (CAPD)患者及 6只雄性新西兰兔腹膜透析模型 ,摇摆和腹部震荡前后透出液内溶质 (D)与血浆中相应溶质 (P)比值 (D/P)及溶质转运面积系数 (MTAC)和引流量的变化。结果 :在震动与非震动组肌酐D/P值及在 45min与 6min具有显著差异 (P <0 0 5 ) ,而两组蛋白质D/P值及引流量比较差异无显著性 (P >0 0 5 )。CAPD患者低频组与高频组 2h和 4h尿素氮D/P值及 2h肌酐D/P值较基础值均明显增加 (P <0 0 1或 0 0 5 ) ,而两组间比较差异无显著性 (P >0 0 5 ) ;蛋白质D/P值及引流量与基础蛋白质D/P值及引流量比较均无差异 (P >0 0 5 )。结论 :摇摆和腹部震荡均能增加小分子尿素氮和肌酐的转运 ,对大分子蛋白质转运及超滤量无影响 ,提示增加CAPD病人的活动能提高腹膜透析的效能。     

Efficacy and Safety of Mineralocorticoid Receptor Antagonists in Kidney Failure Patients Treated with Dialysis: A Systematic Review and Meta-Analysis

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Analysis of Oxygen Transport to Hepatocytes in a Flat-Plate Microchannel Bioreactor

Oxygen transfer to cultured hepatocytes in microchannel parallel-plate bioreactors with and without an internal membrane oxygenator was investigated with a mathematical model and the results were corroborated with fluorescence imaging experiments. The consumption of oxygen by hepatocytes was assumed to follow Michaelis–Menten kinetics. Our simulations indicate that under conditions of low Péclet (Pe) number (<80) and fixed Damkohler number (=0.14, corresponding to rat hepatocytes) the cells are hypoxic in the bioreactor without an internal membrane oxygenator. Under the same conditions, the bioreactor with an internal membrane oxygenator can avoid cell hypoxia by appropriate selection of membrane Sherwood number and/or the gas phase oxygen partial pressure, thus providing greater control of cell oxygenation. At high Pe, both bioreactors are well oxygenated. Experimentally determined oxygen concentrations within the bioreactors were in good qualitative agreement with model predictions. At low Pe, cell surface oxygen depletion was predicted from analytically derived criteria. Hepatocytes with oxygen dependent functional heterogeneity may exhibit optimal function in the bioreactor with the internal membrane oxygenator. © 2001 Biomedical Engineering Society. PAC01: 8717Aa, 8780-y     

Two physically,functionally, and developmentally distinct peritoneal macrophage subsets

The peritoneal cavity (PerC) is a unique compartment within which a variety of immune cells reside, and from which macrophages (MØ) are commonly drawn for functional studies. Here we define two MØ subsets that coexist in PerC in adult mice. One, provisionally called the large peritoneal MØ (LPM), contains approximately 90% of the PerC MØ in unstimulated animals but disappears rapidly from PerC following lipopolysaccharide (LPS) or thioglycolate stimulation. These cells express high levels of the canonical MØ surface markers, CD11b and F4/80. The second subset, referred to as small peritoneal MØ (SPM), expresses substantially lower levels of CD11b and F4/80 but expresses high levels of MHC-II, which is not expressed on LPM. SPM, which predominates in PerC after LPS or thioglycolate stimulation, does not derive from LPM. Instead, it derives from blood monocytes that rapidly enter the PerC after stimulation and differentiate to mature SPM within 2 to 4 d. Both subsets show clear phagocytic activity and both produce nitric oxide (NO) in response to LPS stimulation in vivo. However, their responses to LPS show key differences: in vitro, LPS stimulates LPM, but not SPM, to produce NO; in vivo, LPS stimulates both subsets to produce NO, albeit with different response patterns. These findings extend current models of MØ heterogeneity and shed new light on PerC MØ diversity, development, and function. Thus, they introduce a new context for interpreting (and reinterpreting) data from ex vivo studies with PerC MØ.     

Further findings on the mechanism of cadmium uptake by intestinal mucosal cells (step 1 of Cd absorption)

This work confirms and extends earlier studies on the mechanism of Cd uptake (step 1 of absorption) by the jejunal mucosa of the rat. The Q₁₀ for step 1A, the binding of Cd to the membrane, approximates 1.0. Internalization of bound Cd (step 1B) exhibits a constant Q₁₀ of 1.4 between 0 and 37°C, providing no evidence for a phase shift in the membrane in that range. Chelators which compete for Cd with the membranes thereby inhibit step 1. Membrane-bound Cd behaves kinetically as a single pool, even though only 1/3 participates in step 1B. Binding does not involve reactive -SH groups. Fractional uptake of 5 μM ¹⁰⁹Cd is equally depressed by 250 μM Cd or Zn; the non-specific apparent saturation of Cd uptake can be explained by charge neutralization on the membrane, and does not require postulation of Cd carriers. These findings support the proposed model of jejunal Cd uptake.     

Non-specific uptake of IgG by rat epididymal tubules in vitro

Tubules isolated from the initial segment, caput and corpus regions of the rat epididymis were incubated for 4 h in medium containing rat IgG or bovine-serum-albumin (10 mg ml-1) and processed for light microscopy immunocytochemistry using gold-labelled anti-rat IgG and silver staining or peroxidase/anti-peroxidase techniques. Distribution of IgG was confined to the peritubular matrix only, with no detectable uptake into the epithelium or lumen. In tubules incubated with rat IgG coupled to gold particles as tracer and fixed for electron microscopy, the IgG-gold complex failed to penetrate to the base of the epithelium. When IgG-peroxidase conjugates were used, sparse enzyme activity was localized in small basal and apical vesicles and multivesicular bodies of the principal cells. However, this uptake could not be inhibited by the presence of a 30-fold excess of non-labelled IgG, and the same distribution of enzyme activity was also observed when tubules were incubated with a similar activity of horseradish peroxidase alone. These findings indicate that there is no detectable receptor-mediated transport of IgG across the epididymal epithelium, although non-selective transfer could occur via fluid-phase endocytosis.