Temperature-Related Ultrastructural Changes in Early Stage Amelogenesis in Vascularly Perfused Rat Incisors

1987 ◽  
Vol 1 (2) ◽  
pp. 371-379 ◽  
Author(s):  
Y. Takano ◽  
M. Akai ◽  
S. Matsuo ◽  
S. Wakisaka ◽  
H. Ichikawa ◽  
...  

Vascularly perfused rat incisors were investigated by electron microscopy in order to achieve further definition of the origin and nature of stippled material in developing enamel. A prolonged (20-minute) pre-wash perfusion of the rat with a physiological solution at 37°C prior to perfusion fixation retained good morphology of the secretory ameloblasts and adjacent enamel, showing virtually no extracellular accumulation of granular material. Granular material appeared throughout the developing enamel after pre-wash perfusion at low temperatures (0-2°C), and accumulated in the extensively dilated extracellular spaces between the proximal portions of Tomes' processes, where numerous coated pits and coated vesicles were located. Vascular perfusion at 37°C, preceded by a cold perfusion, abolished the granular material in the developing enamel, whereas the granular material in the extracellular spaces between Tomes' processes remained as huge droplets of dense material. These results indicate that at least a part of the matrix protein of rat incisor developing enamel has the physico-chemical property to dissociate at low temperature during pre-wash perfusion and move toward the enamel surface. Thus, in perfusion-fixed specimens, an intimate relationship between the artifactual formation of stippled material and the temperature of the pre-wash perfusate is suggested.

Author(s):  
H.M. Mazzone ◽  
W.F. Engler ◽  
R. Zerillo ◽  
G.F. Bahr

The nucleopolyhedrosis virus (NPV) of the forest tent cater - pillar (Malacosoma disstria Hubner) has been analyzed in our laboratories. As a representative of the Baculovirus class, the NPV has virus particles enclosed with in a proteinaceous structure, the inclusion body.


2006 ◽  
Vol 17 (9) ◽  
pp. 4051-4062 ◽  
Author(s):  
Michelle R. Gallas ◽  
Mary K. Dienhart ◽  
Rosemary A. Stuart ◽  
Roy M. Long

Many mitochondrial proteins are encoded by nuclear genes and after translation in the cytoplasm are imported via translocases in the outer and inner membranes, the TOM and TIM complexes, respectively. Here, we report the characterization of the mitochondrial protein, Mmp37p (YGR046w) and demonstrate its involvement in the process of protein import into mitochondria. Haploid cells deleted of MMP37 are viable but display a temperature-sensitive growth phenotype and are inviable in the absence of mitochondrial DNA. Mmp37p is located in the mitochondrial matrix where it is peripherally associated with the inner membrane. We show that Mmp37p has a role in the translocation of proteins across the mitochondrial inner membrane via the TIM23-PAM complex and further demonstrate that substrates containing a tightly folded domain in close proximity to their mitochondrial targeting sequences display a particular dependency on Mmp37p for mitochondrial import. Prior unfolding of the preprotein, or extension of the region between the targeting signal and the tightly folded domain, relieves their dependency for Mmp37p. Furthermore, evidence is presented to show that Mmp37 may affect the assembly state of the TIM23 complex. On the basis of these findings, we hypothesize that the presence of Mmp37p enhances the early stages of the TIM23 matrix import pathway to ensure engagement of incoming preproteins with the mtHsp70p/PAM complex, a step that is necessary to drive the unfolding and complete translocation of the preprotein into the matrix.


2015 ◽  
Vol 12 (03) ◽  
pp. 1550013 ◽  
Author(s):  
Siu-Siu Guo ◽  
Dongfang Wang ◽  
Zishun Liu

The concept of structural intensity (SI) is extended to the random domain by introducing a physical quantity denominated random structural intensity (RSI). This quantity is formulated for mechanical systems whose dynamical responses are stochastic due to random excitations. In order to fully characterize the stochastic behavior of a system under random loadings, it is imperative to obtain the probability density function (PDF) of RSI. Based on the elastic theory and the definition of SI, RSI is expressed as functions of system responses. In general, the PDF of system responses is governed by Fokker–Planck–Kolmogorov (FPK) equation under the assumption that random dynamic loadings are idealized as white noise excitations. Therefore, the PDF of RSI is derived with the joint PDF of system responses. In the present study, four demonstrating cases of beams and plates under separately concentrated and uniform random loadings are studied to investigate the properties of RSI. Stationary and non-stationary PDFs of RSI at arbitrary section of beam and plate are obtained. Numerical results show that the PDF of RSI is transient at early stage of stationary loading and then converges to the exact stationary ones as time increases. With the obtained PDFs of RSI, energy transmission path over the beam and plate can be determined, which is guided from the locations with lower probabilities of RSI to the ones with higher probabilities of RSI. Furthermore, virtual energy flow sinks on the plate and beam can be found, which are identified by the locations with the maximum probabilities of RSI.


2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Yuichi Matsushima ◽  
Kazuya Takahashi ◽  
Song Yue ◽  
Yuki Fujiyoshi ◽  
Hideaki Yoshioka ◽  
...  

AbstractHuman ATP-dependent Lon protease (LONP1) forms homohexameric, ring-shaped complexes. Depletion of LONP1 causes aggregation of a broad range of proteins in the mitochondrial matrix and decreases the levels of their soluble forms. The ATP hydrolysis activity, but not protease activity, of LONP1 is critical for its chaperone-like anti-aggregation activity. LONP1 forms a complex with the import machinery and an incoming protein, and protein aggregation is linked with matrix protein import. LONP1 also contributes to the degradation of imported, aberrant, unprocessed proteins using its protease activity. Taken together, our results show that LONP1 functions as a gatekeeper for specific proteins imported into the mitochondrial matrix.


PPAR Research ◽  
2010 ◽  
Vol 2010 ◽  
pp. 1-12 ◽  
Author(s):  
Utpal Sen ◽  
Suresh C. Tyagi

Dysfunction of macro- and microvessels is a major cause of morbidity and mortality in patients with cardio-renovascular diseases such as atherosclerosis, hypertension, and diabetes. Renal failure and impairment of renal function due to vasoconstriction of the glomerular arteriole in diabetic nephropathy leads to renal volume retention and increase in plasma homocysteine level. Homocysteine, which is a nonprotein amino acid, at elevated levels is an independent cardio-renovascular risk factor. Homocysteine induces oxidative injury of vascular endothelial cells, involved in matrix remodeling through modulation of the matrix metalloproteinase (MMP)/tissue inhibitor of metalloproteinase (TIMP) axis, and increased formation and accumulation of extracellular matrix protein, such as collagen. In heart this leads to increased endothelial-myocyte uncoupling resulting in diastolic dysfunction and hypertension. In the kidney, increased matrix accumulation in the glomerulus causes glomerulosclerosis resulting in hypofiltration, increased renal volume retention, and hypertension. PPARγagonist reduces tissue homocysteine levels and is reported to ameliorate homocysteine-induced deleterious vascular effects in diabetes. This review, in light of current information, focuses on the beneficial effects of PPARγagonist in homocysteine-associated hypertension and vascular remodeling in diabetes.


2016 ◽  
Vol 12 (9) ◽  
pp. e1005880 ◽  
Author(s):  
Preeti Bharaj ◽  
Yao E. Wang ◽  
Brian E. Dawes ◽  
Tatyana E. Yun ◽  
Arnold Park ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
J.-C. Cortés ◽  
L. Jódar ◽  
Francisco J. Solís ◽  
Roberto Ku-Carrillo

We introduce infinite matrix products including some of their main properties and convergence results. We apply them in order to extend to the matrix scenario the definition of the scalar gamma function given by an infinite product due to Weierstrass. A limit representation of the matrix gamma function is also provided.


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