PubMed · 10991713
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M L Halperin, D Z Cherney. 2000-09-14. Hypernatremia.. https://doi.org/10.1056/nejm200009143431117
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In skeletal musculature intramyocellular (IMCL) and extramyocellular lipids (EMCL) are stored in compartments of different geometry and experience different magnetic field strengths due to geometrical susceptibility effects. The effect is strong enough to---at least partly---separate IMCL and EMCL contributions in (1)H MR spectroscopy, despite IMCL and EMCL consisting of the same substances. The assessment of intramyocellular lipid stores in skeletal musculature by (1)H MR spectroscopy plays an important role for studying physiological and pathological aspects of lipid metabolism. Therefore, a method using mathematical tools of Fourier analysis is developed to obtain the magnetic field distribution (MFD) from the measured spectra by deconvolution. A reference lipid spectrum is required which was recorded in tibial yellow bone marrow. It is shown that the separation of IMCL contributions can be performed more precisely---compared to other methods---based on the MFD. Examples of deconvolution in model systems elucidate the principle. Applications of the proposed approach on in vivo examinations in m. soleus and m. tibialis anterior are presented. Fitting the IMCL part of the MFD by a Gaussian lineshape with a linewidth kept fixed with respect to the linewidth of creatine and with the assumption of a smooth but not necessarily symmetrical shape for the EMCL part, the only free fit parameter, the amplitude of the IMCL part, is definite and subtraction leads to the EMCL part in the MFD. This procedure is especially justified for the soleus muscle showing a severely asymmetrical distribution which might lead to a marked overestimation of IMCL using common line fitting procedures.
To determine the relationship between phloem transport and changes in phloem water content, we measured temporal and spatial variations in water content and sucrose, glucose and fructose concentrations in phloem samples and phloem exudates of 70- and 30-year-old Norway spruce trees (Picea abies (L.) Karst.). Large temporal and spatial variations in phloem water content (1.4-2.6 mg mg(dw)(-1)) and phloem total sugar concentration (31-70 mg g(dw)(-1)) paralleled each other (r(2) = 0.83, P < 0.0001 for the temporal profile and r(2) = 0.96, P < 0.008 for the spatial profile), indicating that phloem water content depends on the total amount of sugar to be transferred. Changes in phloem water content were unrelated to changes in bark thickness. Maximum changes in phloem water content calculated from dendrometer readings were only 8-11% of the maximum measured changes in phloem water content, indicating that reversible changes in bark thickness did not reflect changes in internal water relations. We also studied the relationship between xylem sap velocity and changes in bark thickness in 70-year-old trees during summer 1999 and winter 1999-2000. Sap flow occurred sporadically throughout the winter, but there was no relationship between bark shrinkage or swelling and sap velocity. In winter, mean daily xylem sap velocity was significantly correlated with mean daily vapor pressure deficit and air temperature (P < 0.0001, in both cases). Changes in bark thickness corresponded with both short- and long-term changes in relative humidity, in both winter and summer. Under controlled conditions at > 0 degrees C, changes in relative humidity alone caused changes in thickness of boiled bark samples. Because living bark of Norway spruce trees contains large areas with crushed and dead sieve cell zones-up to 24% of the bark is air-filled space-we suggest that this space can compensate for volume changes in living phloem cells independently of total tissue water content. We conclude that changes in bark thickness are not indicative of changes in either phloem water capacitance or xylem sap flow.
The invasive phenotype, characteristic of malignancy, is found in multiple transformed populations with widely varying genotypes. The authors hypothesize that this genetic heterogeneity and instability precludes mechanisms of tumour invasion requiring consistent, coordinated production of one or more proteins or other macromolecules. Instead, this model assumes that the genetically disordered, unstable populations found in tumours must employ a simple mechanism of invasion that arises from one common trait of all transformed cells--reversion to a phenotype more primitive (less differentiated) than the tissue of origin. Specifically, this approach focuses on primitive metabolic pathways with preferential use of glycolysis for energy production. Mathematical models of invasive cancer based on tumour-induced acidification of the microenvironment are presented. Using population ecology and diffusion-reaction models, it is shown that normal tissue adjacent to the tumour edge is subjected to an extracellular pH that is significantly lower than normal. This leads to degradation of the interstitial matrix, loss of intercellular gap junctions and cell necrosis. Tumour cells have an optimal extracellular pH less than that of normal cells and are thus able to thrive in the acidic microenvironment expanding into the space of the dying normal tissue. The model is consistent with extant data on the tumour microenvironment as well as clinical data relating increasing tumour invasiveness with elevated glucose utilization and lactate content. It predicts well-established phenomena in tumorigenesis such as the adenoma-carcinoma sequence and the critical role of angiogenesis in the invasive phenotype. An acellular gap at the tumour host interface is also predicted and can be demonstrated in pathologic specimens. Novel treatment approaches based on this model are discussed.