Objectives. Recent studies suggest the presence of a hereditary form of benign prostatic hyperplasia (H-BPH). This study was undertaken to characterize the histopathologic features of BPH in these ...men.
Methods. Because study subjects with H-BPH were young (mean age 59 years) and had a large prostate (mean prostate weight 61 g), we compared the histopathologic findings in these men with those in two different control groups: (1) age-matched control subjects (mean age 59 years; mean prostate weight 31 g), and (2) prostate weight-matched control subjects (mean age 70 years; mean prostate weight 61 g). Using a color video image analysis system, we morphometrically determined stromal/epithelial ratios in histologic sections taken from 12 men with H-BPH, 36 age-matched control subjects, and 36 prostate weight-matched control subjects.
Results. The stromal/epithelial ratio was 2.6±1.4 in the men with H-BPH, 2.7±1.7 in the age-matchedcontrol subjects, and 1.7±0.9 in the prostate weight-matched control subjects. Regression analysis, which controlled for the differences in prostate weight or patient age between men with H-BPH and age-matched and prostate weight-matched control subjects, respectively, revealed a significant difference between men with H-BPH and prostate weight-matched control subjects (
P=0.015) but no difference from age-matched control subjects (
P=0.36).
Conclusions. The larger prostates in young men with H-BPH are characterized by a higher stromal/epithelial ratio than are similar-sized prostates in older men with sporadic BPH. This finding gives rise to speculation that H-BPH is associated with an increase in stromal elements.
The hillslope rainfall-outflow interactions, groundwater fluxes, and hydrological balance were examined in the small mountainous headwater catchment Uhlířská, the Jizera Mountains, the Czech ...Republic. The hillslope soil profile is formed by paleozoic crystalline bedrock overlaid by shallow highly permeable shallow Cambisol, and by thick saturated glacial deposits in the valley, overlaid by Histosol. A quick communication of the vadose zone with the granitic bedrock via preferential subsurface flowpaths is hypothesised, in agreement with the observation of storm-caused instant water transformation to outflow through the permeable Cambisol. A quick response of a high magnitude outflow occurs regularly, although the surface runoff is very rare. Standard climatic and hydrological monitoring in the Uhlířská catchment is supplemented by the measurements of the soil moisture, soil pore water suction, subsurface hillslope stormflow in the vadose zone, and water table fluctuation in the saturated subsurface, and is accompanied by water sampling for the analyses of the contents of the isotope 18O and 2H and geochemical tracer silica in the form of SiO2. The episode based isotopic data serve for the separation of the outflow hydrograph to determine the contributions of the event and pre-event water in the hypodermic hillslope outflow and in the catchment outflow. The variation of silica content in the water cycle components was examined to assess the contributions from the soil profile and the aquifer. Up to 75% of the event catchment runoff was assigned to pre-event water, of which about 50% had been stored in the shallow soil subsurface on the hillslopes. The hypothesis was confirmed that the hillslope soil layers control the distribution of the flow into the groundwater recharge and/or the shallow subsurface flow during the rainfallrunoff episode.
We attempted to determine the clinical and biological characteristics of familial benign prostatic hyperplasia (BPH).
Urinary flow rate, prostate size, symptom score, serum prostate specific antigen, ...testosterone and dihydrotestosterone were measured in subjects who participated in the nationwide Merck phase III finasteride clinical trial. Findings in the 69 men with familial BPH (3 or more family members with BPH, including the proband) were compared to those in the 345 with no family history of BPH. Logistic regression was used to detect relationships between familial BPH, and these variables before and after 5 alpha-reductase inhibition with finasteride.
Familial BPH was characterized by large prostate size. Mean prostate volume in men with familial and sporadic BPH was 82.7 and 55.5 ml., respectively (p <0.001). Other clinical findings, including serum androgen levels and response to finasteride, were similar in familial and sporadic BPH. The frequency of familial BPH in patients with prostate size in the largest and smallest deciles was 46 and 13%, respectively.
Familial BPH in this group of patients was associated with large prostate size, normal serum androgen levels and normal response to 5 alpha-reductase inhibition. A genetic factor responsible for familial BPH may exert its influence through androgen independent control of prostatic growth.
In ischemic or hypoxic tissues, elevated Ca2+ levels have emerged as one of the main damaging agents among other Ca2+-independent mechanisms of cellular injury. Because mitochondria, besides the ...endoplasmic reticulum, play a key role in the maintainance of cellular Ca2+ homeostasis, alterations in the mitochondrial Ca2+ content (Ca2+m) were monitored in addition to changes in cytosolic Ca2+ concentration (Ca2+i) during metabolic inhibition (MI) in renal epithelial Madin-Darby canine kidney (MDCK) cells. Ca2+i and Ca2+m were monitored via, respectively, fura 2 and rhod 2 measurements. MI induced an increase in Ca2+i reaching 631 ± 78 nM in 20 min, followed by a decrease to 118 ± 9 nM in the next 25 min. A pronounced drop in cellular ATP levels and a rapid increase in intracellular Na+ concentrations in the first 20 min of MI excluded Ca2+ efflux in the second phase via plasma membrane ATPases or Na+/Ca2+ exchangers (NCE). Mitochondrial rhod 2 intensities increased to 434 +/- 46% of the control value during MI, indicating that mitochondria sequester Ca2+ during MI. The mitochondrial potential (m) was lost in 20 min of MI, excluding mitochondrial Ca2+ uptake via the m-dependent mitochondrial Ca2+ uniporter after 20 min of MI. Under Na+-free conditions, or when CGP-37157, a specific inhibitor of the mitochondrial NCE, was used, no drop in Ca2+i was seen during MI, whereas the MI-induced increase in mitochondrial rhod 2 fluorescence was strongly reduced. To our knowledge, this study is the first to report that in metabolically inhibited renal epithelial cells mitochondria take up Ca2+ via the NCE acting in the reverse mode. PUBLICATION ABSTRACT
In ischemic or hypoxic tissues, elevated Ca
2+
levels have emerged as one of the main damaging agents among other Ca
2+
-independent mechanisms of cellular injury. Because mitochondria, besides the ...endoplasmic reticulum, play a key role in the maintainance of cellular Ca
2+
homeostasis, alterations in the mitochondrial Ca
2+
content (Ca
2+
m
) were monitored in addition to changes in cytosolic Ca
2+
concentration (Ca
2+
i
) during metabolic inhibition (MI) in renal epithelial Madin-Darby canine kidney (MDCK) cells. Ca
2+
i
and Ca
2+
m
were monitored via, respectively, fura 2 and rhod 2 measurements. MI induced an increase in Ca
2+
i
reaching 631 ± 78 nM in ∼20 min, followed by a decrease to 118 ± 9 nM in the next ∼25 min. A pronounced drop in cellular ATP levels and a rapid increase in intracellular Na
+
concentrations in the first 20 min of MI excluded Ca
2+
efflux in the second phase via plasma membrane ATPases or Na
+
/Ca
2+
exchangers (NCE). Mitochondrial rhod 2 intensities increased to 434 ± 46% of the control value during MI, indicating that mitochondria sequester Ca
2+
during MI. The mitochondrial potential (ΔΨ
m
) was lost in 20 min of MI, excluding mitochondrial Ca
2+
uptake via the ΔΨ
m
-dependent mitochondrial Ca
2+
uniporter after 20 min of MI. Under Na
+
-free conditions, or when CGP-37157, a specific inhibitor of the mitochondrial NCE, was used, no drop in Ca
2+
i
was seen during MI, whereas the MI-induced increase in mitochondrial rhod 2 fluorescence was strongly reduced. To our knowledge, this study is the first to report that in metabolically inhibited renal epithelial cells mitochondria take up Ca
2+
via the NCE acting in the reverse mode.
PDF
