Influence of the renal lower pole anatomy and mid-renal-zone classification in successful approach to the calices during flexible ureteroscopy.

PURPOSE: The aim of this paper is to analyze if the anatomy type of the collector system (CS) limits the accessibility of flexible ureteroscopy (FUR) in the lower pole. METHODS: We analyzed the pyelographies of 51 patients submitted to FUR and divided the CS into four groups: A1-kidney midzone (KM) drained by minor calices (Mc) that are dependent on the superior or on the inferior caliceal groups; A2-KM drained by crossed calices; B1-KM drained by a major caliceal group independent both of the superior and inferior groups, and B2-KM drained by Mc entering directly into the renal pelvis. We studied the number of calices, the angle between the lower infundibulum and renal pelvis, and the angle between the lower infundibulum and the inferior Mc. With the use of a flexible ureteroscope, the access attempt was made to all of lower pole calices. Averages were statistically compared using the ANOVA and Unpaired T test (p < 0.05). RESULTS: We found 14 kidneys of A1 (27.45 %); 4 of A2 (7.84 %); 17 of B1 (33.33 %); and 16 of B2 (31.37 %). The LIP was >90° in 31 kidneys (60.78 %) and between 61° and 90° in 20 kidneys (39.22 %). We did not find angles smaller than 60°. The group A1 presented 48 Mc and the UF was able to access 42 (87.5 %); the group A2 had 11 Mc and the UF was able to access 7 (63.64 %); the group B1 had 48 Mc and the UF was able to access 41 (85.42 %) and in group B2 we observed 41 Mc and the UF could access 35 (85.36 %). There was no statistical difference in the accessibility between the groups (p = 0.2610). CONCLUSIONS: Collecting system with kidney midzone drained by crossed calices presented the lower accessibility rate during FUR.

Lower pole anatomy and mid-renal-zone classification applied to flexible ureteroscopy: experimental study using human three-dimensional endocasts.

PURPUSE: The aim of this study was to analyze the anatomy of the inferior pole collecting system and the mid-renal-zone classification in human endocasts applied to flexible ureteroscopy. METHODS: 170 three-dimensional polyester resin endocasts of the kidney collecting system were obtained from 85 adult cadavers. We divided the endocasts into four groups: A1--kidney midzone (KM), drained by minor calices (mc) that are dependent on the superior or the inferior caliceal groups; A2--KM drained by crossed calices; B1--KM drained by a major caliceal group independent of both the superior and inferior groups; and B2--KM drained by mc entering directly into the renal pelvis. We studied the number of calices, the angle between the lower infundibulum and renal pelvis and the angle between the lower infundibulum and the inferior mc (LIICA). Means were statistically compared using ANOVA and the unpaired T test (p < 0.05). RESULTS: We found 57 (33.53 %) endocasts of group A1; 23 (13.53 %) of group A2; 59 (34.71 %) of group B1; and 31 (18.23 %) of group B2. The inferior pole was drained by four or more calices in 84 cases (49.41 %), distributed into groups as follows: A1 = 35 cases (41.67 %); A2 = 18 (21.43 %); B1 = 22 (26.19 %); and B2 = 9 (10.71 %). Perpendicular mc were observed in 15 cases (8.82 %). We did not observe statistical differences between the LIICA in the groups studied. CONCLUSIONS: Collector systems with kidney midzone drained by minor calices that are dependent on the superior or on the inferior caliceal groups presented at least two restrictive anatomical features. The mid-renal-zone classification was predictive of anatomical risk factors for lower pole ureteroscopy difficulties.

Autophagy signaling in hypertrophied muscles of diabetic and control rats.

Autophagy plays a vital role in cell homeostasis by eliminating nonfunctional components and promoting cell survival. Here, we examined the levels of autophagy signaling proteins after 7 days of overload hypertrophy in the extensor digitorum longus (EDL) and soleus muscles of control and diabetic rats. We compared control and 3-day streptozotocin-induced diabetic rats, an experimental model for type 1 diabetes mellitus (T1DM). EDL muscles showed increased levels of basal autophagy signaling proteins. The diabetic state did not affect the extent of overload-induced hypertrophy or the levels of autophagy signaling proteins (p-ULK1, Beclin-1, Atg5, Atg12-5, Atg7, Atg3, LC3-I and II, and p62) in either muscle. The p-ULK-1, Beclin-1, and p62 protein expression levels were higher in the EDL muscle than in the soleus before the hypertrophic stimulus. On the contrary, the soleus muscle exhibited increased autophagic signaling after overload-induced hypertrophy, with increases in Beclin-1, Atg5, Atg12-5, Atg7, Atg3, and LC3-I expression in the control and diabetic groups, in addition to p-ULK-1 in the control groups. After hypertrophy, Beclin-1 and Atg5 levels increased in the EDL muscle of both groups, while p-ULK1 and LC3-I increased in the control group. In conclusion, the baseline EDL muscle exhibited higher autophagy than the soleus muscle. Although TDM1 promotes skeletal muscle mass loss and strength reduction, it did not significantly alter the extent of overload-induced hypertrophy and autophagy signaling proteins in EDL and soleus muscles, with the two groups exhibiting different patterns of autophagy activation.

In Vivo Electrical Stimulation for the Assessment of Skeletal Muscle Contractile Function in Murine Models.

Skeletal muscle electrical stimulation is commonly used for clinical purposes, assisting recovery, preservation, or even improvement of muscle mass and function in healthy and pathological conditions. Additionally, it is a useful research tool for evaluation of skeletal muscle contractile function. It may be applied in vitro, using cell culture or isolated fibers/muscles, and in vivo, using human subjects or animal models (neuromuscular electrical stimulation - NMES). This chapter focuses on the electrical stimulation of the sciatic nerve as a research method for evaluation of the contractile properties of murine hind limb muscles. Variations of this protocol allow for the assessment of muscle force, fatigue resistance, contraction and relaxation times, and can be used as a model of contraction-induced muscle injury, reactive oxygen species production, and muscle adaptation to contractile activity.

Hypertrophy Stimulation at the Onset of Type I Diabetes Maintains the Soleus but Not the EDL Muscle Mass in Wistar Rats.

Diabetes mellitus induces a reduction in skeletal muscle mass and strength. Strength training is prescribed as part of treatment since it improves glycemic control and promotes increase of skeletal muscle mass. The mechanisms involved in overload-induced muscle hypertrophy elicited at the establishment of the type I diabetic state was investigated in Wistar rats. The purpose was to examine whether the overload-induced hypertrophy can counteract the hypotrophy associated to the diabetic state. The experiments were performed in oxidative (soleus) or glycolytic (EDL) muscles. PI3K/Akt/mTOR protein synthesis pathway was evaluated 7 days after overload-induced hypertrophy of soleus and of EDL muscles. The mRNA expression of genes associated with different signaling pathways that control muscle hypertrophy was also evaluated: mechanotransduction (FAK), Wnt/ß-catenin, myostatin, and follistatin. The soleus and EDL muscles when submitted to overload had similar hypertrophic responses in control and diabetic animals. The increase of absolute and specific twitch and tetanic forces had the same magnitude as muscle hypertrophic response. Hypertrophy of the EDL muscle from diabetic animals mostly involved mechanical loading-stimulated PI3K/Akt/mTOR pathway besides the reduced activation of AMP-activated protein kinase (AMPK) and decrease of myostatin expression. Hypertrophy was more pronounced in the soleus muscle of diabetic animals due to a more potent activation of rpS6 and increased mRNA expression of insulin-like growth factor-1 (IGF-1), mechano-growth factor (MGF) and follistatin, and decrease of myostatin, MuRF-1 and atrogin-1 contents. The signaling changes enabled the soleus muscle mass and force of the diabetic rats to reach the values of the control group.

SOCS3 expression in SF1 cells regulates adrenal differentiation and exercise performance.

Many hormones/cytokines are secreted in response to exercise and cytokine signaling may play a pivotal role in the training adaptations. To investigate the importance of cytokine signaling during vertical ladder climbing, a resistance exercise model, we produced mice lacking SOCS3 protein exclusively in steroidogenic factor-1 (SF1) cells (SF1 Socs3 KO mice). SF1 expression is found in steroidogenic cells of the adrenal cortex and gonads, as well as in neurons of the ventromedial nucleus of the hypothalamus. Histological markers of the fetal adrenal zone (or X-zone in rodents) were still present in adult males and postpartum SF1 Socs3 KO females, suggesting a previously unrecognized effect of SOCS3 on the terminal differentiation of the adrenal gland. This change led to a distinct distribution of lipid droplets along the adrenal cortex. Under basal conditions, adult SF1 Socs3 KO mice exhibited similar adrenal weight, and plasma ACTH and corticosterone concentrations. Nonetheless, SF1 Socs3 KO mice exhibited a blunted ACTH-induced corticosterone secretion. The overall metabolic responses induced by resistance training remained unaffected in SF1 Socs3 KO mice, including changes in body adiposity, glucose tolerance and energy expenditure. However, training performance and glucose control during intense resistance exercise were impaired in SF1 Socs3 KO mice. Furthermore, a reduced counter-regulatory response to 2-deoxy-d-glucose was observed in mutant mice. These findings revealed a novel participation of SOCS3 regulating several endocrine and metabolic aspects. Therefore, cytokine signaling in SF1 cells exerts an important role to sustain training performance possibly by promoting the necessary metabolic adjustments during exercise.

Effect of shock wave reapplication on urinary N-acetyl-beta-glucosaminidase in canine kidney.

OBJECTIVE: Renal tubular damage can be assessed with the aid of urinary dosing of N-acetyl-beta-glucosaminidase (NAG) and it is possible to demonstrate a significant correlation between shock wave and damage to renal parenchyma. The objective of this study was to assess the effect of shock wave reapplication over urinary NAG in canine kidney. MATERIALS AND METHODS: The authors submitted 10 crossbred dogs to 2 applications of 2000 shock waves in a 24-hour interval in order to assess urinary NAG values after 12, 24, 36 and 48 hours. RESULTS: Twelve hours following the first shockwave application there was an increase in NAG of 6.47 +/- 5.44 u/g creatinine (p < 0.05). Twelve hours and 24 h following the second application there was no increase in the urinary enzyme, -2.56 +/- -7.36 u/g creatinine and 2.89 +/- -7.27 u/g creatinine, respectively (p > 0.05). CONCLUSION: Shock wave reapplication with a 24-hour interval did not cause any increase in urinary NAG.

Effect of shock wave reapplication on urinary n-acetyl-beta-glucosaminidase in canine kidney

OBJECTIVE: Renal tubular damage can be assessed with the aid of urinary dosing of N-acetyl-beta-glucosaminidase (NAG) and it is possible to demonstrate a significant correlation between shock wave and damage to renal parenchyma. The objective of this study was to assess the effect of shock wave reapplication over urinary NAG in canine kidney. MATERIALS AND METHODS: The authors submitted 10 crossbred dogs to 2 applications of 2000 shock waves in a 24-hour interval in order to assess urinary NAG values after 12, 24, 36 and 48 hours. RESULTS: Twelve hours following the first shockwave application there was an increase in NAG of 6.47 ± 5.44 u/g creatinine (p < 0.05). Twelve hours and 24 h following the second application there was no increase in the urinary enzyme, - 2.56 ± - 7.36 u/g creatinine and 2.89 ± - 7.27 u/g creatinine, respectively (p > 0.05). CONCLUSION: Shock wave reapplication with a 24-hour interval did not cause any increase in urinary NAG.