Volumetric Analysis of Carpal Bones by Sex with 3D Slicer Software Program / Análisis Volumétrico de los Huesos del Carpo por Sexo con el Programa de Software 3D Slicer

SUMMARY: In this study, we aim to share the volumes of the carpal bone and the ratio of these volumes to the total volume of wrist bones from Computed Tomography (CT) images obtained from individuals of different ages and sex using 3D Slicer. Right wrist CT images of 0.625 mm slice thickness of 42 healthy individuals (21 female, 21 male) of both sexes were included in our study. Volume calculations were made by loading the images into 3D Slicer, an open-source software package. In this study, mean capitate volume was the largest in both sexes (male 3479.9±679.2; female 2207.1±272.1 mm3), while pisiform had the smallest mean volume (male 810.0±141.2; female 566.6±97.7 mm3). This order was ordered from largest to smallest as hamate, scaphoid, trapezium, lunate, triquetrum, trapezoid, and pisiform. According to this study, carpal bone volumes were larger in males than in females (p0.05). In this study, it was seen that carpal bone volume differed according to sex. However, it was observed that the bone volumes of both sexes took up the same amount in the total bone volume. This information will be very useful in sex determination, 3D anatomical material creation, implant applications and reconstructive surgery.

Nuestro objetivo fue determinar los volúmenes de los huesos del carpo y la relación entre estos volúmenes y el volumen total de estos huesos a partir de imágenes de TC obtenidas de individuos de diferentes edades y sexos utilizando 3D Slicer. En el estudio se incluyeron imágenes de TC del carpo de la mano derecha de los participantes en el estudio, con un grosor de corte de 0,625 mm, en 42 individuos sanos (21 mujeres, 21 hombres) de ambos sexos. Los cálculos de volumen se realizaron cargando las imágenes en 3D Slicer, un paquete de software de código abierto. El volumen medio del hueso capitado fue el mayor en ambos sexos (hombre 3479,9 ± 679,2; mujer 2207,1 ± 272,1 mm3), mientras que el hueso pisiforme tuvo el volumen medio más pequeño (hombre 810,0 ± 141,2; mujer 566,6 ± 97,7 mm3). De mayor a menor el volumen de los otros huesos fue: hamato, escafoides, trapecio, lunato, piramidal, trapezoide y pisiforme. Según este estudio, los volúmenes óseos del carpo eran mayores en hombres que en mujeres (p0,05). En este estudio se observó que el volumen de los huesos del carpo difería según el sexo. Sin embargo, se observó que los volúmenes óseos de ambos sexos ocuparon la misma cantidad del volumen óseo total. Esta información será de gran utilidad en la determinación del sexo, creación de material anatómico 3D, aplicaciones de implantes y cirugía reconstructiva.

Burned spinal cord in acidotic cerebrospinal fluid during subarachnoid hemorrhage: Experimental study.

OBJECTIVE: We investigated the effect of carotid body ischemia-induced cerebrospinal fluid acidosis on spinal cord during subarachnoid hemorrhage (SAH). METHODS: Twenty-three hybrid rabbits were divided into three groups: control (n = 5), Sham (injected with 0.5 ml isotonic) (n = 6), and the SAH (n = 12) (injected with 0.5 ml autologous blood into the 4th ventricle) and then monitored for 3 weeks. Cerebrospinal fluid pH and degenerated ependymal cell density and volume of cervical central canal were analyzed. RESULTS: The mean cervical central canal volumes, degenerated ependymal cells densities, and cerebrospinal pH values were 1.056 ± 0.053 mm3-6 ± 2 per mm2-7.342 ± 0.034, 1.321 ± 0.12 mm3-35 ± 9 per mm2-7.314 ± 0.056, and 1.743 ± 0.245 mm3-159 ± 24 per mm2-7.257 ± 0.049 in the Control, Sham, and SAH groups, respectively. The more degenerated carotid body neuron density induced decreased cerebrospinal fluid pH values (p < 0.0001) could result in the more ependymal cells desquamation (p < 0.0005) and central canal dilatation (p < 0.00001). CONCLUSION: Increased neurodegeneration of carotid bodies can reduce cause cerebrospinal fluid pH-induced ependymal cell degeneration and central canal dilatation following SAH.

OBJETIVO: El objetivo de este estudio fue investigar el efecto de la isquemia inducida del cuerpo carotideo por la acídosis de líquido cefalorraquídeo en la médula espinal durante una hemorragia subaracnoidea (SAH). METODO: Conejos híbridos (n = 23) fueron divididos en Control (n = 5), Sham (inyectados con 0.5 mil de solución isotónica) (n = 6), y SAH (n = 12) (inyectados en el 4º ventrículo con 0.5 ml de sangre autológa) y monitoreados por tres semanas. Se analizaron: El pH del líquido cerebro espinal, la densidad de las células ependimarias y el volúmen del canal cervical central. RESULTADOS: La media del volumen del canal cervical central, la densidad de las células ependimarias degeneradas y los valores de pH fueron 1.056 + 0.053 mm3-6 + 2 per mm2-7.342 + 0.034, 1.321 + 0.12 mm3-35 + 9 per mm2-7.314 + 0.056 y 1.743 + 0.245 mm3-159 + 24 per mm2-7.257 + 0.049 en los grupos Control, Sham y SHA, respectivamente. La mayor densidad inducida de la neurona del cuerpo carotideo degenerado, disminuyó los valores de pH del líquido cefalorraquideo lo que podría dar como resultado un aumento en la descamación de las células ependimarias asi como la dilatación del canal central. CONCLUSIÓN: Un aumento en la neurodegeneración del cuerpo carotideo puede reducir la degeneración de los ependimocitos y la dilatacióm del canal central siguiendo SAH.

Is Uric Acid elevation a random finding or a causative agent of diabetic nephropathy?

OBJECTIVE: In this study, we aimed to analyze the relationship between serum uric acid (UA) and microalbuminuria as a marker of renal injury in type 2 diabetes mellitus. METHODS: A total of 100 patients with type 2 diabetes mellitus were enrolled in the study. Participants were divided into two groups according to the urinary microalbumin/creatinine ratio: diabetic nephropathy and non-nephropathy group. UA and microalbuminuria were compared between the study groups. RESULTS: Serum UA levels of diabetic nephropathy patients were significantly higher than those in the non-nephropathy group (UA in patients with diabetic nephropathy groups: 6.3 (1.82) mg/dl, UA in patients of the non-nephropathic group: 4.85 (1.92) mg/dl) (p<0.001). There was a correlation between microalbuminuria and UA (r=0.238). This correlation was statistically significant (p=0.017). CONCLUSION: UA levels may be an important predictor of nephropathy in diabetic patients.

Is Uric Acid elevation a random finding or a causative agent of diabetic nephropathy?

SUMMARY OBJECTIVE In this study, we aimed to analyze the relationship between serum uric acid (UA) and microalbuminuria as a marker of renal injury in type 2 diabetes mellitus. METHODS A total of 100 patients with type 2 diabetes mellitus were enrolled in the study. Participants were divided into two groups according to the urinary microalbumin/creatinine ratio: diabetic nephropathy and non-nephropathy group. UA and microalbuminuria were compared between the study groups. RESULTS Serum UA levels of diabetic nephropathy patients were significantly higher than those in the non-nephropathy group (UA in patients with diabetic nephropathy groups: 6.3 (1.82) mg/dl, UA in patients of the non-nephropathic group: 4.85 (1.92) mg/dl) (p<0.001). There was a correlation between microalbuminuria and UA (r=0.238). This correlation was statistically significant (p=0.017). CONCLUSION UA levels may be an important predictor of nephropathy in diabetic patients.

RESUMO OBJETIVO O objetivo deste estudo foi analisar a relação entre o ácido úrico sérico e a microalbuminúria como marcador de lesão renal no diabetes mellitus tipo 2. MÉTODOS Um total de 100 pacientes com diabetes mellitus tipo 2 foram inscritos no estudo. Os grupos de estudo foram divididos em dois, de acordo com a relação microalbumina/creatinina na urina: nefropatia diabética e grupo não nefropático. UA e microalbuminúria foram comparados entre os grupos de estudo. RESULTADOS Os níveis séricos de AU de pacientes com nefropatia diabética foram significativamente maiores do que o grupo sem nefropatia (AU em pacientes com grupos de nefropatia diabética: 6,3 (1,82) mg/dl, AU em pacientes com grupos não nefropáticos: 4,85 (1,92) mg/dl ) (p<0,001). Houve correlação entre microalbuminúria e AU (r=0,238). Essa correlação foi estatisticamente significativa (p=0,017). CONCLUSÃO Os níveis de AU podem ser um importante preditor de nefropatia em pacientes diabéticos.

New determinants for casual peripheral mechanism of neurogenic lung edema in subarachnoid hemorrhage due to ischemic degeneration of vagal nerve, kidney and lung circuitry. Experimental study1.

PURPOSE: To evaluate whether there is a relationship between renal artery vasospasm related low glomerular density or degeneration and neurogenic lung edema (NLE) following subarachnoid hemorrhage. METHODS: This study was conducted on 26 rabbits. A control group was formed of five animals, a SHAM group of 5 to which saline and a study group (n=16) injected with homologous blood into the sylvian cisterna. Numbers of degenerated axons of renal branches of vagal nerves, atrophic glomerulus numbers and NLE scores were recorded. RESULTS: Important vagal degeneration, severe renal artery vasospasm, intrarenal hemorrhage and glomerular atrophy observed in high score NLE detected animals. The mean degenerated axon density of vagal nerves (n/mm2), atrophic glomerulus density (n/mm3) and NLE scores of control, SHAM and study groups were estimated as 2.40±1.82, 2.20±1.30, 1.80±1.10, 8.00±2.24, 8.80±2.39, 4.40±1.14 and 154.38±13.61, 34.69±2.68 and 12.19±1.97 consecutively. Degenerated vagal axon, atrophic glomerulus and NLE scores are higher in study group than other groups and the differences are statistically meaningful (p<0.001). CONCLUSION: Vagal complex degeneration based glomerular atrophy have important roles on NLE following SAH which has not been extensively mentioned in the literature.

New determinants for casual peripheral mechanism of neurogenic lung edema in subarachnoid hemorrhage due to ischemic degeneration of vagal nerve, kidney and lung circuitry. Experimental study

Purpose:To evaluate whether there is a relationship between renal artery vasospasm related low glomerular density or degeneration and neurogenic lung edema (NLE) following subarachnoid hemorrhage.Methods:This study was conducted on 26 rabbits. A control group was formed of five animals, a SHAM group of 5 to which saline and a study group (n=16) injected with homologous blood into the sylvian cisterna. Numbers of degenerated axons of renal branches of vagal nerves, atrophic glomerulus numbers and NLE scores were recorded.Results:Important vagal degeneration, severe renal artery vasospasm, intrarenal hemorrhage and glomerular atrophy observed in high score NLE detected animals. The mean degenerated axon density of vagal nerves (n/mm2), atrophic glomerulus density (n/mm3) and NLE scores of control, SHAM and study groups were estimated as 2.40±1.82, 2.20±1.30, 1.80±1.10, 8.00±2.24, 8.80±2.39, 4.40±1.14 and 154.38±13.61, 34.69±2.68 and 12.19±1.97 consecutively. Degenerated vagal axon, atrophic glomerulus and NLE scores are higher in study group than other groups and the differences are statistically meaningful (p<0.001).Conclusion:Vagal complex degeneration based glomerular atrophy have important roles on NLE following SAH which has not been extensively mentioned in the literature.(AU)

New determinants for casual peripheral mechanism of neurogenic lung edema in subarachnoid hemorrhage due to ischemic degeneration of vagal nerve, kidney and lung circuitry. Experimental study

Abstract Purpose: To evaluate whether there is a relationship between renal artery vasospasm related low glomerular density or degeneration and neurogenic lung edema (NLE) following subarachnoid hemorrhage. Methods: This study was conducted on 26 rabbits. A control group was formed of five animals, a SHAM group of 5 to which saline and a study group (n=16) injected with homologous blood into the sylvian cisterna. Numbers of degenerated axons of renal branches of vagal nerves, atrophic glomerulus numbers and NLE scores were recorded. Results: Important vagal degeneration, severe renal artery vasospasm, intrarenal hemorrhage and glomerular atrophy observed in high score NLE detected animals. The mean degenerated axon density of vagal nerves (n/mm2), atrophic glomerulus density (n/mm3) and NLE scores of control, SHAM and study groups were estimated as 2.40±1.82, 2.20±1.30, 1.80±1.10, 8.00±2.24, 8.80±2.39, 4.40±1.14 and 154.38±13.61, 34.69±2.68 and 12.19±1.97 consecutively. Degenerated vagal axon, atrophic glomerulus and NLE scores are higher in study group than other groups and the differences are statistically meaningful (p<0.001). Conclusion: Vagal complex degeneration based glomerular atrophy have important roles on NLE following SAH which has not been extensively mentioned in the literature.