Dissectional Orientation: Morphological Variations of Teres Minor Muscle and its Nerve Supply

SUMMARY: The teres minor is one of the rotator cuff muscles that comprise the superior margin of the quadrangular space. Quadrangular space syndrome (QSS) refers to the entrapment or compression of the axillary nerve and the posterior humeral circumflex artery in the quadrangular space, often caused by injuries, dislocation of the shoulder joint, etc. Patients who fail the primary conservative treatments and have persistent symptoms and no pain relief for at least six months would be considered for surgical interventions for QSS. This cadaveric study of 17 cadavers (males: 9 and females: 8) was conducted in the Gross Anatomy Laboratory at the Department of Anatomy, Faculty of Medicine Siriraj Hospital, Mahidol University. The cadavers were preserved in a 10 % formaldehyde solution and obtained ethical approval by the ethical commission of the Siriraj Institutional Review Board. The morphology of the teres minor muscle-tendon junction, the bifurcation type of the axillary nerve, and the length and number of the terminal branches of the nerve to the teres minor were documented. Specimens with quadrangular space contents and surrounding muscles that had been destroyed were excluded from the study. The results showed that 47.06 % of the specimens had type A bifurcation, 47.06 % had type B bifurcation, and the remaining 5.88 % had type C bifurcation. It was observed that 58.82 % had nonclassic muscle-tendon morphology, while 41.18 % were classic. The average length of the terminal branches of the nerve to the teres minor in males was 1.13 cm, with the majority having two branches. For females, many showed one terminal branch with an average length of 0.97 cm. Understanding the differences in anatomical variations can allow for a personalized treatment plan prior to quadrangular space syndrome surgical procedures and improve the recovery of postsurgical interventions for patients.

El músculo redondo menor es uno de los músculos del manguito rotador que comprende el margen superior del espacio cuadrangular. El síndrome del espacio cuadrangular (QSS) se refiere al atrapamiento o compresión del nervio axilar y la arteria circunfleja humeral posterior en el espacio cuadrangular, a menudo causado por lesiones, dislocación de la articulación humeral, entre otros. En los pacientes en los que fracasan los tratamientos conservadores primarios y presentan síntomas persistentes y ningún alivio del dolor durante al menos seis meses se considerarían para intervenciones quirúrgicas para QSS. Este estudio cadavérico de 17 cadáveres (hombres: 9 y mujeres: 8) se llevó a cabo en el Laboratorio de Anatomía Macroscópica del Departamento de Anatomía de la Facultad de Medicina del Hospital Siriraj de la Universidad Mahidol. Los cadáveres se conservaron en una solución de formaldehído al 10 % y obtuvieron la aprobación ética de la comisión ética de la Junta de Revisión Institucional de Siriraj. Se documentó la morfología de la unión músculo-tendón del músculo redondo menor, el tipo de bifurcación del nervio axilar y la longitud y el número de las ramas terminales del nervio para el músculo redondo menor. Se excluyeron del estudio los especímenes con contenido de espacios cuadrangulares y músculos circundantes que habían sido destruidos. Los resultados mostraron que el 47,06 % de los especímenes presentó bifurcación tipo A, el 47,06 % una bifurcación tipo B y el 5,88 % restante una bifurcación tipo C. Se observó que el 58,82 % presentaba una morfología músculo-tendinosa no clásica, mientras que el 41,18 % era clásica. La longitud pmedia de los ramos terminales del nervio hasta el músculo redondo menor en los hombres era de 1,13 cm, y la mayoría tenía dos ramos. En el caso de las mujeres, mostraron un ramo terminal con una longitud promedio de 0,97 cm. Comprender las diferencias en las variaciones anatómicas puede permitir un plan de tratamiento personalizado antes de los procedimientos quirúrgicos del síndrome del espacio cuadrangular y mejorar la recupe- ración de las intervenciones posquirúrgicas de los pacientes.

Uncontrolled Diabetes with Underlying Structural Changes in the Atrioventricular Node / Diabetes no Controlada con Cambios Estructurales Subyacentes en el Nodo Atrioventricular

SUMMARY: Diabetic cardiomyopathy, characterized by diabetes mellitus (DM) -induced cardiac muscular abnormalities, is a strong inducer of impaired cardiac contraction and arrhythmia. Atrioventricular block, a serious type of arrhythmia resulting from interruption of cardiac impulse conduction via the atrioventricular node (AVN), frequently occurs among diabetic patients. However, details of structural changes in AVN in DM remain poorly explained. Here, this study defined the effects of DM on the morphological remodeling of the AVN in male Sprague Dawley rats induced by intraperitoneal injection of streptozotocin (60 mg/kg body weight). At 24 weeks, the pathological changes in the AVN were assessed by light microscopy (LM) and transmission electron microscopy (TEM). Under LM, the AVN in diabetic rats became a less compact mass and exhibited the intracellular vacuolation. The nodal cells were more varied in sizes with the absence or shrinkage of nuclei and clear cytoplasm compared to the control. The collagen content significantly increased in relation to the presence of myofibroblasts. Consistent with LM, TEM images of the diabetic nodal cells revealed several signs of cell damage, such as mitochondrial changes, deterioration of cell organelles, gap junction internalization, and cell separation. Furthermore, changes in AVN innervation, evidenced by damaged Schwann cells and axons, were also found. These results indicated alterations in important components in the AVN during diabetic condition, which may lead to the impairment of electrical conduction, causing abnormal cardiac functions in diabetic patients.

La miocardiopatía diabética, caracterizada por anomalías musculares cardíacas inducidas por diabetes mellitus (DM), es un fuerte inductor de alteración de la contracción cardíaca y arritmia. El bloqueo atrioventricular, un tipo grave de arritmia resultante de la interrupción de la conducción del impulso cardíaco a través del nodo atrioventricular (NAV), se produce con frecuencia entre los pacientes diabéticos. Sin embargo, los detalles de los cambios estructurales en NAV en DM siguen estando pobremente explicados. Aquí, este estudio definió los efectos de la DM en la remodelación morfológica del NAV en ratas macho Sprague Dawley inducidas por inyección intraperitoneal de estreptozotocina (60 mg/kg de peso corporal). A las 24 semanas, los cambios patológicos en el NAV se evaluaron mediante microscopía óptica (MO) y microscopía electrónica de transmisión (MET). Bajo MO, el NAV en ratas diabéticas se convirtió en una masa menos compacta y exhibió la vacuolización intracelular. Las células nodales tenían tamaños más variados con ausencia o contracción de núcleos y citoplasma claro en comparación con el control. El contenido de colágeno aumentó significativamente en relación con la presencia de miofibroblastos. De acuerdo con MO, las imágenes MET de las células nodales diabéticas revelaron varios signos de daño celular, como cambios mitocondriales, deterioro de los orgánulos celulares, internalización de uniones comunicantes y separación celular. Además, también se encontraron cambios en la inervación del NAV, evidenciados por schwannocitos y axones dañados. Estos resultados indicaron alteraciones en componentes importantes en el NAV durante la condición diabética, lo que puede conducir al deterioro de la conducción eléctrica, causando funciones cardíacas anormales en estos pacientes.

Altered Chief Cell Morphology in the Gastric Gland of Streptozotocin-Diabetic Rats

SUMMARY: Diabetes mellitus (DM) is a metabolic disorder with rising incidences worldwide. Gastric symptoms of DM have been reported, including nausea, vomiting, bloating, and epigastric pain. Moreover, acute to chronic gastritis and atrophic gastritis occur in DM can affect the chief cells of the gastric gland. Chief cells are vital because of their ability to digest and separate vitamin B12 from protein. Lack of vitamin B12 leads to impaired DNA synthesis and abnormal metabolism in red blood cells, and eventually leading to pernicious anemia. Furthermore, decreased vibratory and positional senses, numbness, ataxia with subacute combined degeneration, and dementia are present in pernicious anemic patients. Twenty-four male adult Sprague-Dawley rats were used in this study. The rats were divided into control (n = 12) and diabetic (n = 12) groups. The rats were further separated into two categories: short-term (4 weeks) and long-term (24 weeks) groups. DM model was induced by manually injecting intraperitoneally with streptozotocin in citrate buffer at a dose of 60 mg/kg body weight. The same amount of buffer was injected into the control group. After sacrifice, three regions of the stomach (the cardia, body, and pylorus) were dissected. Histopathology was performed by staining with toluidine blue. Image analysis was used to quantify the zymogen granule accumulation in chief cells. The data were compared between the control and DM rats in each period using Student's t-test. In addition, transmission electron microscopy (TEM) was also used to examine the ultrastructures. There was a significant decrease in the percentage of zymogen granules in DM rats. Under TEM, the destructions of mitochondria, rough endoplasmic reticulum, and Golgi apparatus in the DM rat were observed in the chief cells. In rats with uncontrolled diabetes, there is damage to the chief cells all over the area of the stomach, affecting digestion and malabsorption of vitamin B12. Therefore, this result helps clinicians recognize that diabetic patients with gastric symptoms may have hidden pernicious anemia.

La diabetes mellitus (DM) es un trastorno metabólico con incidencia creciente a nivel mundial. Se han informado síntomas gástricos de DM, que incluyen náuseas, vómitos, distensión abdominal y dolor epigástrico. Además, la gastritis aguda a crónica y la gastritis atrófica que ocurren en la DM pueden afectar las células principales de la glándula gástrica. Las células principales son vitales debido a su capacidad para digerir y separar la vitamina B12 de las proteínas. La falta de vitamina B12 conduce a una síntesis de ADN deteriorada y un metabolismo anormal en los glóbulos rojos, lo que eventualmente conduce a una anemia perniciosa. Además, los pacientes con anemia perniciosa presentan disminución de los sentidos vibratorio y posicional, entumecimiento, ataxia con degeneración combinada subaguda y demencia. En este estudio se usaron 24 ratas Sprague-Dawley macho adultas. Las ratas se dividieron en grupos control (n = 12) y diabéticas (n = 12). Las ratas se separaron además en dos categorías: grupos a corto plazo (4 semanas) y a largo plazo (24 semanas). El modelo de DM se indujo inyectando manualmente por vía intraperitoneal estreptozotocina en tampón de citrato a una dosis de 60 mg/kg de peso corporal. Se inyectó la misma cantidad de tampón en el grupo control. Después del sacrificio, se disecaron tres regiones del estómago (cardias, cuerpo y píloro). La histopatología se realizó mediante tinción con azul de toluidina. El análisis de imágenes se utilizó para cuantificar la acumulación de gránulos de zimógeno en las células principales. Los datos se compararon entre las ratas control y DM en cada período utilizando la prueba t de Student. Además, se utilizó microscopía electrónica de transmisión (TEM) para examinar la ultraestructura celular. Hubo una disminución significativa en el porcentaje de gránulos de zimógeno en ratas DM. Bajo TEM, se observaron en las células principales las destrucción de las mitocondrias, del retículo endoplásmico rugoso y del complejo golgiense en la rata DM. En ratas con diabetes no controlada, hay daño en las células principales de toda el área del estómago, lo que afecta la digestión y la malabsorción de vitamina B12. Por lo tanto, este resultado ayuda a los médicos a reconocer que los pacientes diabéticos con síntomas gástricos pueden tener una anemia perniciosa oculta.

Identification of Variation in the Extrahepatic Arterial System of Thai Cadavers / Identificación de la Variación en el Sistema Arterial Extrahepático de Cadáveres Tailandeses

SUMMARY: Liver transplantation (LT) is the treatment of choice for decompensated liver cirrhosis. In the LT procedure, an adequate arterial supply is required for anastomosis to prevent postoperative necrosis and maintain hepatic parenchymal functions. The extrahepatic arterial system is primarily responsible for carrying oxygenated blood from the heart, 25 % of total cardiac output. Normally, the celiac trunk gives off the common hepatic artery. The common hepatic artery branches into the hepatic artery proper and supplies blood to the hepatic parenchyma. Recognizing the anatomical variations of the hepatic artery proper is essential for the planning and implementation of LT. The extrahepatic arterial variations are hard to study in live humans because of the limitations of human rights. Studying cadavers can solve this problem. This study investigates the distribution of normal, accessory, and replaced hepatic arteries proper by dissecting Thai cadavers (n = 152; males = 82 and females = 70) in the Gross Anatomy Laboratory at the Department of Anatomy, Faculty of Medicine Siriraj Hospital, Mahidol University. The cadavers were preserved in a 10 % formaldehyde solution. The exclusion criteria for liver specimens were cirrhosis, liver carcinoma, including hepatocellular carcinoma and cholangiocarcinoma, and other liver masses. Accordingly, the extrahepatic arterial system was conventionally dissected and identified at the porta hepatis. The extrahepatic arterial system was identified and documented in terms of features of normal distribution and variations, such as accessory or replaced hepatic arteries. There were 75 % normal type, 18.42 % accessory left hepatic arteries (aLHA), 1.32 % replaced left hepatic arteries (rLHA), 0.66 % accessory right hepatic arteries (aRHA), 1.32 % of replaced right hepatic arteries (rRHA), 1.97 % of aLHA and aRHA, and 1.32 % aortic type. The identification of variations in the hepatic artery system is essential to detection of distribution patterns. This knowledge is crucial for promoting LT.

El trasplante hepático (TH) es el tratamiento de elección para la cirrosis hepática descompensada. En el procedimiento de TH, se requiere un suministro arterial adecuado para la anastomosis para prevenir la necrosis postoperatoria y mantener las funciones del parénquima hepático. El sistema arterial extrahepático es el principal responsable de transportar sangre oxigenada desde el corazón, el 25 % del gasto cardíaco total. Normalmente, el tronco celíaco da origen a la arteria hepática común. La arteria hepática común se ramifica en la arteria hepática propia y suministra sangre al parénquima hepático. Reconocer las variaciones anatómicas de la arteria hepática es fundamental para la planificación e implementación del TH. Las variaciones arteriales extrahepáticas son difíciles de estudiar en humanos vivos debido a las limitaciones de los derechos humanos. El estudio de cadáveres puede resolver este problema. Este estudio investiga la distribución de las arterias hepáticas normales, accesorias y aberrantes mediante la disección de cadáveres tailandeses (n = 152; hombres = 82 y mujeres = 70) en el Laboratorio de Anatomía Macroscópica del Departamento de Anatomía, Facultad de Medicina del Hospital Siriraj, Mahidol. Los cadáveres se conservaron en una solución de formaldehído al 10 %. Los criterios de exclusión para las muestras de hígado fueron cirrosis, carcinoma hepático, incluidos el carcinoma hepatocelular y el colangiocarcinoma, y otras masas hepáticas. En consecuencia, el sistema arterial extrahepático se diseccionó e identificó convencionalmente en el hilio hepático. El sistema arterial extrahepático se identificó y documentó en términos de características de distribución normal y variaciones, como arterias hepáticas accesorias. Hubo 75 % tipo normal, 18,42 % arterias hepáticas izquierdas accesorias (aLHA), 1,32 % arterias hepáticas izquierdas aberrantes (LHAr), 0,66 % arterias hepáticas derechas accesorias (aRHA), 1,32 % arterias hepáticas derechas aberrantes (ARHr), 1,97 % de aLHA y aRHA, y 1,32 % de tipo aórtico. La identificación de variaciones en el sistema de la arteria hepática es esencial para la detección de patrones de distribución. Este conocimiento es crucial para promover LT.

The effects of early diabetes on duodenal alterations in the rats / Efectos de la diabetes temprana sobre las alteraciones duodenales en ratas

SUMMARY: Diabetes mellitus (DM) mainly affects functional changes in the duodenum, which plays an important role in the digestion and absorption of food. The impairment of duodenal function contributes to malnutrition, abdominal bloating and pain in diabetic patients. Thus, this study aimed to investigate the histological alterations and quantitative measurements of duodenal structures in the early stage of streptozotocin (STZ)-induced diabetic rats. Eight male Sprague-Dawley rats were divided into three control and five diabetic rats. Diabetes was induced by a single intraperitoneal dose of 60 mg/kg STZ. After four weeks of diabetic induction, the duodenum was prepared for histological study and morphometric analysis. In diabetic rats, there were deformed villi with disrupted surface epithelium and mildly distorted shapes of crypts, together with an increase in villus height and crypt depth. The epithelial cells detached from their underlying basement membrane. The goblet cells decreased in number, whereas an increased number of Cellula panethensis (Paneth cells) with pale-stained eosinophilic granules occurred in the DM group. A diabetic thickened submucosal layer was observed as enhanced duodenal glands (Brunner's glands) hypertrophy and collagen accumulation. These findings indicated that histopathologic lesions of the duodenum developed in the early stage of diabetes. The destruction of villi, crypts, and epithelium may affect digestion and absorption. The structural changes in goblet and Cellula panethensis and duodenal glands may be associated with malfunction to protect duodenal mucosa from bacteria and stomach acid. These conditions can worsen the quality of life in diabetic individuals, leading to complications such as maldigestion, malabsorption, and duodenal ulcer.

RESUMEN: La diabetes mellitus (DM) afecta principalmente a cambios funcionales en el duodeno, que juega un papel importante en la digestión y absorción de los alimentos. El deterioro de la función duodenal contribuye a la desnutrición, distensión abdominal y dolor en pacientes diabéticos. Por lo tanto, este estudio tuvo como objetivo estudiar las alteraciones histológicas y determinar las mediciones cuantitativas de las estructuras duodenales en la etapa temprana de ratas diabéticas inducidas por estreptozotocina (STZ). Ocho ratas macho Sprague-Dawley fueron distribuidas en dos grupos: tres ratas control y cinco diabéticas. La diabetes se indujo mediante una dosis intraperitoneal única de 60 mg/kg de STZ. Después de cuatro semanas de inducción, se preparó el duodeno para estudio histológico y análisis morfométrico. En ratas diabéticas, había vellosidades deformadas con epitelio superficial destruido y formas ligeramente distorsionadas de las criptas, junto con un aumento en la altura de las vellosidades y la profundidad de las criptas. Las células epiteliales se encontraban separadas de la membrana basal subyacente. Las células caliciformes habían disminuido en número, mientras que en el grupo DM se produjo un aumento en el número de Cellula panethensis (células de Paneth) con gránulos eosinofílicos teñidos pálidos. Se observó una capa submucosa engrosada con aumento de la hipertrofia de las glándulas duodenales (glándulas de Brunner) y acumulación de colágeno. Estos hallazgos indican que las lesiones histopatológicas del duodeno se desarrollaron en la etapa temprana de la diabetes. La destrucción de vellosidades, criptas y epitelio puede afectar la digestión y la absorción. Los cambios estructurales en Cellula panethensis y glándulas duodenales pueden estar asociados con un mal funcionamiento en la protección de la mucosa duodenal tanto de las bacterias como del ácido gástrico. Estas condiciones pueden empeorar la calidad de vida de las personas diabéticas y provocar complicaciones como mala digestión, malabsorción y úlcera duodenal.

Small bronchiolar histopathological changes related to prolonged diabetes / Pequeños cambios histopatológicos bronquiolares relacionados con la diabetes prolongada

SUMMARY: Diabetes mellitus increases the risk of developing chronic obstructive pulmonary disease (COPD). The small bronchiole is a prominent site of airflow obstruction that causes increased airway resistance in patients with the COPD. Therefore, the histological and ultrastructural changes in small bronchioles in streptozotocin (STZ)-induced chronic diabetes were determined. Twenty-four weeks after STZ induction, rats were sacrificed, and the right and left lungs were collected for examination by light and electron microscopy. The alterations to the small bronchioles were the same in both lungs of these diabetic rats. The bronchiolar epithelial cells, both ciliated and secretory club cells, showed pyknotic nuclei and damaged cytoplasmic organelles. Increased thickening of the bronchiolar wall occurred in diabetic rats due to smooth muscle layer thickening, inflammatory cell infiltration, and increased numbers of myofibroblasts with collagen deposition.These results indicated that chronic diabetes caused extreme damage to small bronchioles, which may lead to chronic small airway obstruction and ultimately increase the likelihood of COPD progression. This basic knowledge provides a better understanding of the progression of pathogenesis in the small airways of patients with prolonged diabetes.

RESUMEN: La diabetes mellitus aumenta el riesgo de desarrollar enfermedad pulmonar obstructiva crónica (EPOC). El bronquiolo es un sitio prominente de obstrucción del flujo de aire que causa una mayor resistencia de las vías respiratorias en pacientes con EPOC. Por lo tanto, se determinaron los cambios histológicos y ultraestructurales en los bronquiolos en la diabetes crónica inducida por estreptozotocina (STZ). 24 semanas después de la inducción de STZ, se sacrificaron las ratas y se analizaron los pulmones derecho e izquierdo por microscopía óptica y electrónica. Las alteraciones de los pequeños bronquiolos fueron las mismas en ambos pulmones de estas ratas diabéticas. Las células epiteliales bronquiolares, tanto ciliadas como secretoras, mostraban núcleos picnóticos y orgánelos citoplasmáticos dañados. Se produjo un aumento del engrosamiento de la pared bronquiolar en ratas diabéticas debido al engrosamiento de la capa de músculo liso, infiltración de células inflamatorias y un mayor número de miofibroblastos con colágeno. Estos resultados indicaron que la diabetes crónica causaba daño extremo a los pequeños bronquiolos, lo que puede conducir a una obstrucción crónica de las vías respiratorias pequeñas y además aumentar la probabilidad de progresión de la EPOC. Esta información proporcionará un mejor conocimiento de la patogénesis en las vías respiratorias pequeñas de los pacientes con diabetes prolongada.

Modifications of adrenal gland ultrastructure in streptozotocin-induced diabetic model rats / Modificaciones de la ultraestructura de la glándula suprarrenal en ratas modelo diabéticas inducidas por estreptozotocina

SUMMARY: The adrenal gland has been associated with the development of classical symptoms in diabetes mellitus (DM), including intensive polyuria and hyperglycemia. During DM, there are hormonal changes in the adrenal gland. Ultrastructural changes of adrenocortical and adrenal medulla cells and their effects on adrenocorticomedullary interaction have not been fully investigated. This study evaluated adrenocortical and adrenal medullary cells and adrenocorticomedullary interactions at ultrastructural levels in a streptozotocin-induced DM model, using transmission electron microscopy. Fifteen male, Sprague-Dawley rats were divided into diabetic model (n = 10) and control (n = 5) groups. Rats were sacrificed at four weeks after induction. The nuclei of some diabetic cortical cells were found to be irregularly shaped. In the cytoplasm, increased numbers of mitochondria and dilated smooth endoplasmic reticulum were observed. However, lipid droplets decreased in the DM model animals. The filopodia of diabetic cortical cells extended to contact the fenestrated capillary and other cortical cells and losses of gap junctions were also observed. Alterations of diabetic chromaffin cells resulted in similar appearances, consisting of irregularly shaped nuclei, swollen mitochondria, distended rough endoplasmic reticulum, and disrupted chromaffin vesicles. Examining adrenocorticomedullary interactions showed that the diabetic cortical chromaffin cells resembled those in the medulla. In the DM model group, collagen fibril depositions were observed between adrenal cells, especially near cell interactions. The filopodia of diabetic cortical cells were larger than those observed for diabetic adrenocorticomedullary interactions and adrenal cortex. These adrenal gland ultrastructural modifications represent contributions to the basic knowledge necessary for investigations of adrenal gland impairment during the early diagnosis of DM patients.

RESUMEN: La glándula suprarrenal se ha asociado con el desarrollo de síntomas clásicos en la diabetes mellitus (DM), que incluyen poliuria intensiva e hiperglucemia. Durante la DM, hay cambios hormonales en la glándula suprarrenal. Los cambios ultraestructurales de las células adrenocorticales y de la médula suprarrenal y sus efectos sobre la interacción adrenocorticomedular no se han investigado completamente. Este estudio evaluó las células adrenocorticales y de la médula suprarrenal y las interacciones adrenocorticomedulares a niveles ultraestructurales en un modelo de DM inducida por estreptozotocina, utilizando microscopía elec- trónica de transmisión. Se dividieron quince ratas macho Sprague- Dawley en grupos de modelo diabético (n = 10) y de control (n = 5). Las ratas se sacrificaron cuatro semanas después de la inducción. Se encontró que los núcleos de algunas células corticales diabéticas tenían una forma irregular. En el citoplasma, se observó un mayor número de mitocondrias y retículo endoplásmico liso dilatado. Sin embargo, las gotitas de lípidos disminuyeron en los animales modelo DM. Los filopodios de las células corticales diabéticas se extendieron para entrar en contacto con el capilar fenestrado y otras células corticales y también se observaron pérdidas de uniones gap. Las alteraciones de las células cromafines diabéticas dieron como resultado apariencias similares, que consistían en núcleos de forma irregular, mitocondrias inflamadas, retículo endoplásmico rugoso distendido y vesículas cromafines rotas. El examen de las interacciones adrenocorticomedulares mostró que las células cromafines corticales diabéticos se parecían a las de la médula. En el grupo del modelo de DM, se observaron depósitos de fibrillas de colágeno entre las células suprarrenales, especialmente cerca de las interacciones celulares. Los filopodios de las células corticales diabéticas eran más grandes que los observados para las interacciones adrenocorticomedulares diabéticas y la corteza suprarrenal. Estas modificaciones ultraestructurales de la glándula suprarrenal contribuyen al conocimiento básico para las investigaciones referente al deterioro de la glándula en el diagnóstico temprano de pacientes con DM.

Altered oligodendrocytes in spinal enlargements of streptozotocin diabetic rats / Oligodendrocitos alterados en la intumescencia espinal de ratas diabéticas con estreptozotocina

SUMMARY: Disturbances of sensory and motor nerve conduction velocity in the spinal cord as well as degenerated myelin sheaths are observed in diabetic patients and animal models. Indeed, oligodendrocytes (OLs), which are important neuroglial cells, generate myelin in the central nervous system. Spinal enlargement, including cervical and lumbar enlargements, innervates all limbs. Thus, the purposes of this study were to examine and compare the ultrastructural alterations of OLs in spinal enlargements of streptozotocin (STZ)- induced diabetic rats and controls. Thirteen male Sprague-Dawley rats were induced with STZ in citrate buffer and six control rats were injected with the same buffer solution. All rats were sacrificed after inductions at four (short-term DM) and twenty-four weeks (long-term DM). The selected spinal enlargements were processed for transmission electron microscopy. The OL alterations in both the cervical and lumbar enlargements were apparently the same. In short-term DM, the nuclei of OLs became swelled with chromatin clumping. Cytoplasmic organelles were moderately damaged. In long-term DM, OLs contained shrinkage nuclei with thick heterochromatin clumping. Severely degenerated mitochondria with disrupted cristae and broken membranes were observed. Moreover, distended and fragmented rough endoplasmic reticulum were observed, and large clear areas were present in the cytoplasm. Additionally, the loosening, splitting, and destruction of myelin lamellae were found. This study can provide important preliminary information about the alteration of OLs in the spinal cords of diabetic patients, which might be involve in the impairments of sensory and motor conduction velocities in these individuals.

RESUMEN: En pacientes diabéticos y modelos animales se observan alteraciones de la velocidad de conducción nerviosa sensorial y motora en la médula espinal, así como vainas de mielina degeneradas. De hecho, los oligodendrocitos (OL), que son importantes células neurogliales, generan mielina en el sistema nervioso central. La intumescencia espinal, a nivel cervical y lumbar, inerva los miembros. Por lo tanto, los propósitos de este estudio fueron examinar y comparar las alteraciones ultraestructurales de los OL en la intumescencia espinal de ratas diabéticas inducidas por estreptozotocina (STZ) y controles. Se indujeron trece ratas macho Sprague-Dawley con STZ en tampón citrato y se inyectaron seis ratas de control con la misma solución tampón. Todas las ratas se sacrificaron después de la inducción a las cuatro (DM a corto plazo) y a las veinticuatro semanas (DM a largo plazo). Las ampliaciones de la columna seleccionadas se procesaron para microscopía electrónica de transmisión. Las alteraciones de OL en las intumescencias cervical y lumbar eran aparentemente las mismas. En la DM a corto plazo, los núcleos de los OL se hincharon con la acumulación de cromatina. Los orgánulos citoplasmáticos sufrieron daños moderados. En la DM a largo plazo, los OL contenían núcleos de contracción con aglutinación de heterocromatina gruesa. Se observaron mitocondrias severamente degeneradas con crestas y membranas rotas. Además, se observó un retículo endoplásmico rugoso distendido y fragmentado, y estaban presentes grandes áreas claras en el citoplasma. Además, se encontraron el aflojamiento, la división y la destrucción de las laminillas de mielina. Este estudio puede proporcionar información preliminar importante sobre la alteración de los OL en la médula espinal de los pacientes diabéticos, que podría estar involucrada en las alteraciones de las velocidades de conducción sensorial y motora en estos individuos.

Cerebellar synaptopathy in streptozotocin-induced diabetic rats / Sinaptopatía cerebelosa en ratas diabéticas inducidas por estreptozotocina

SUMMARY: There is an increasing amount of evidence that supports the diabetic complications of the central nervous system structure and function. The cerebellum, which is one of the primary structure derived from the hindbrain, plays an important role in motor control, motor coordination, and non-motor functions, such as cognitive processing. The synapse is a critical structure that regulates neuronal communication, and well-defined afferent and efferent fibre connections in the cerebellum help in maintaining the proper working order. Thus, the present study sought to investigate the long-term effects of diabetes-induced synaptopathy in the cerebellum, using both histological and ultrastructural studies. Twenty Sprague-Dawley male rats were divided randomly into control and diabetic groups, and diabetes was then induced through a single intraperitoneal injection of streptozotocin (60 mg/kg body weight). Six month later, the rats were sacrificed and the cerebellum was removed. Light and electron microscopic examinations showed a degeneration of Purkinje cells (Neuron purkinjense) with shrunken cells, pyknotic nuclei, and synaptopathy, including the reduction in synapse density, number of synaptic vesicles, and maturation of synapses in the molecular layer of diabetic cerebellum. The disruptions in synaptic profiles, which observed in the diabetic condition, could be related to cerebellar dysfunction, thus leading to the defects in coordinated movement, balance, as well as cognitive learning and memory.

RESUMEN: Actualmente existe una creciente evidencia que apoya las complicaciones diabéticas de la estructura y función del sistema nervioso central. El cerebelo, una de las estructuras primarias del cerebro posterior, desempeña un papel importante en el control motor, la coordinación motora y las funciones no motoras, tanto como en el procesamiento cognitivo. La sinapsis es una estructura crítica que regula la comunicación neuronal y las conexiones de fibras aferentes y eferentes bien definidas en el cerebelo, ayudan a mantener el funcionamiento correcto. Por lo tanto, en el presente estudio se investigaron los efectos a largo plazo de la sinaptopatía inducida por la diabetes en el cerebelo, utilizando estudios histológicos y ultraestructurales. Veinte ratas SpragueDawley macho se dividieron al azar en grupos de control y diabetes, se indujó la diabetes a través de una inyección intraperitoneal única de estreptozotocina (60 mg / kg de peso corporal). Seis meses después, se sacrificaron las ratas y se extrajo el cerebelo. Los exámenes de microscopías óptica y electrónica mostraron una degeneración de las neuronas purkinjenses (células de Purkinje), con células reducidas, núcleos picnóticos y sinaptopatía, como también la densidad reducida de sinapsis, el número de vesículas sinápticas y la maduración de las sinapsis en la capa molecular del cerebelo de las ratas diabéticas. Las interrupciones en los perfiles sinápticos, que se observaron en la condición diabética, podrían estar relacionadas con la disfunción cerebelosa, lo que lleva a defectos en el movimiento coordinado, el equilibrio, así como al aprendizaje cognitivo y la memoria.

Cardiac ultrastructure in streptozotocin-induced diabetic rats.

Objective: To examine the alterations of four cardiac chambers in the streptozotocin (STZ)-induced diabetic rats by using light and transmission electron microscopies Materials and Methods: Eleven STZ-induced diabetic and six control adult male Sprague-Dawley rats were applied. After the induction for 24 weeks, all heart chambers were proceeded with histological and ultrastructural techniques. Results: In the diabetes, swollen endothelial and mesothelial cells laid on thick basal lamina, and their cytoplasm comprised numerous pinocytotic vesicles, vacuoles, and dilated rER. The subendocardial and subepicardial layers were enlarged with accumulations of collagen fibrils. Both cardiac myocytes and Purkinje fibers became hypertrophy. The interstitial fibrosis, contraction band necrosis, and infiltrations of lymphocytes and macrophages were observed in some areas of myocardium. The myocardium of the left ventricle showed interstitial hemorrhage. In both cardiac myocytes and Purkinje fibers, the arrangement of sarcomere was irregular with lost myofilaments. Moreover, swollen mitochondria with disrupted cristae were examined and increased in number. The number of specific atrial granules decreased in the atrial cardiac myocytes. Increased lipid droplets and myelin figures were seen in the myocytes. The intercalated disc was disrupted in some portions. The capillary lumen was narrowed due to swollen endothelial cells with thick basal lamina. Conclusion: DM causes numerous cardiac alterations in all three layers of four chambers. This study provides an important basic knowledge for understanding the pathological changes and options for further therapeutic treatment of cardiac complications in the diabetic patients.

Ultrastructural changes of hepatic stellate cells in streptozotocin-induced diabetic rats.

Background: Thirty to forty per cent of diabetic patients develops liver cirrhosis. The hepatic stellate cells (HSCs) play an essential role in development of liver fibrosis. Objective: The goal of this study was to demonstrate histological and ultrastructural changes of HSCs in the streptozotocin (STZ)-induced diabetic rats by using light (LM) and transmission electron microscopies (TEM). Materials and Methods: Thirteen male Sprague-Dawley rats were used. Diabetic rats (n=8) were induced by intraperitoneal injection of STZ (60 mg/kg) in citrate buffer (pH 4.5). Each control rat (n=5) was injected with an equal volume of the buffer. The animals were sacrificed at 24 weeks. Liver specimens were examined by utilizing two approaches of LM and TEM, respectively. Results: Under LM observation, most shape of the diabetic HCSs was spindle. Moreover, there were more numerous collagen fibers in the perisinusoidal space of diabetes. By using TEM, the number of HSCs in diabetic group significantly increased. Furthermore, the HSCs in the diabetic group obviously changed into myofibroblast-like cells. The lipid droplets in the cytoplasm noticeably declined in number, which were replaced by collagen fibers. In addition, dilatation of rER and Golgi complex, increasing in number of mitochondria, and binucleated nuclei occurred in the diabetic group. Also, the collagen fibers were accumulated in diabetic perisinusoidal spaces. Conclusion: These new observations provide a research perspective on ultrastructural changes of diabetic HSCs in developing liver cirrhosis, which is more than previously considered. This perspective may have important implications for improved therapeutic treatment.

Effects of streptozotocin-induced diabetes on lingual histological changes in the rats.

Background: Many studies suggest that taste disorders and tongue lesions associate with diabetes mellitus (DM). However, the lingual histopathology underlying impairments in taste sensation, swallowing and speaking in the DM is poorly examined. Objective: The present study aimed to clarify histological changes of the tongues in streptozotocin (STZ)-induced diabetic and control rats by using light microscopy. Materials and Methods: Eight male adult Sprague-Dawley rats; five STZ (60 mg/kg)-induced diabetic and three control rats, were studied. At 24 weeks after the induction, tongues were collected and processed by conventional histological technique with Masson’s trichrome staining. Results: In the DM, thickness of epithelium reduced, whereas that of keratin raised. Moreover, loss of characteristic layering was found. These cells became loss of chromatin. Furthermore, total numbers of taste buds in all types of lingual papillae per a tongue significantly decreased, when compared to those in the control. In both diabetic lamina propria and muscular layer, there were collagen fibers accumulations, numerous inflammatory cells, and swollen endothelial cells with narrowing of capillary lumen. In the muscular layer, average sizes of intrinsic skeletal muscle cells in all zones of diabetic tongue were significantly smaller than those in the control. Conclusion: It is possible that changes in histological characteristics of the tongue are important mechanisms underlying the development of taste disorders, impairments of swallowing and speaking in diabetic patients.

Renal microvascular changes in streptozotocin-induced, long-termed diabetic rat.

OBJECTIVE: To investigate the renal microvascular changes in streptozotocin (STZ)-induced, long-termed diabetic rat. MATERIAL AND METHOD: Twelve male Sprague-Dawley rats were used. Each diabetic rat (n = 8) was induced by an intraperitoneal injection of STZ (60 mg/kg) in citrate buffer (pH 4.5). Control rats (n = 4) were injected intraperitoneally with the same amount of the buffer. The animals were sacrificed at 20 weeks after the injections. The kidneys were processed for conventional light microscopy (LM) and vascular corrosion cast technique with scanning electron microscopy (SEM). RESULTS: Under LM, it was found that the glomerular sizes intensively decreased in the long-termed diabetic rat. The thickening of Bowman's basement membrane was demonstrated. Additionally, there were macrophages and capsular drop lesions in renal corpuscles of long-termed diabetes. The sizes of proximal and distal tubules were markedly destroyed, when compared to the control. Moreover, the epithelial necrosis of vacuolated renal tubules was observed. By using vascular corrosion cast with SEM, the glomerular microvascular sizes in the long-termed diabetes were significantly decreased that corresponded to the result under LM. Furthermore, the size of peritubular capillaries decreased. Concerning to vasa recta in the long-termed diabetes, these vessels ran tortuously and decreased in size. CONCLUSION: Renal microvascular changes, observed in STZ-induced diabetic rats, mimic human diabetic nephropathy (DN). Additionally, the pathological changes of the renal tubules were investigated. Therefore, the present study provides an important basic knowledge for understanding the processes in developing DN, as well as for further study of the therapeutic treatment.

Renal Microvasculature in Lylei’s flying fox (Pteropus lylei).

Objective: The purpose of this study was to elucidate the renal microvasculature of Lylei’s flying fox. Methods: The kidneys of twelve adult Lylei’s flying foxes of both sexes were processed by using vascular corrosion cast technique combined with SEM. Results: It was found that arcuate arteries at the corticomedullary junctions give off several interlobular arteries, which run perpendicularly into the renal cortex. The interlobular artery branches into two sets of vessels. Firstly, aglomerular arteriole divides into capsular and peritubular capillary plexus without forming glomeruli. Secondly, an afferent arteriole, a branch of the interlobular artery, breaks into the glomerular capillary plexus that gathers to form a single efferent arteriole. An efferent arteriole gives rise to a peritubular capillary plexus and vasa recta. A peritubular capillary forms a plexus among renal tubules. Vasa recta are straight vessels that run parallel to Henle’s loops and collecting ducts in the outer medulla. In addition, vasa recta form U- shaped loops in the inner medulla. Moreover, the fenestrated type of capillaries is observed. It was found that high numbers of the fenestration were seen in the glomerular capillary plexus and venous limbs of vasa recta in the outer medulla. In contrast, fewer knobs were presented in the loops of vasa recta in the inner medulla and peritubular capillary plexus. Both peritubular capillary plexus and vasa recta collect the blood into interlobular and arcuate veins. Conclusion: In this investigation, the aglomerular arteriole might be an important shunting of the blood, while this animal alters the position immediately. With the advantages of this technique, fenestrated capillaries are demonstrated which are related to the functions of each tubule. Moreover, the microvascular patterns of the kidney in this animal are similar to that in human. Therefore, it is a suitable model for renal microvascular investigation.

Adrenal microvasculature in the Lylei’s flying fox (Pteropus lylei).

Objective: The purpose of this study was to elucidate the microvasculature of the adrenal glands in the Lylei’s flying fox. Methods: The adrenal glands of the Lylei’s flying foxes were processed in the histological technique and vascular corrosion cast technique combined with the SEM. Results: Upon reaching the gland, the adrenal arteries divided into the cortical and medullary arteries. Firstly, the cortical arteries gave off subcapsular and true cortical capillary plexuses. Few loop cortical arteries were observed. At the corticomedullary junction, true cortical capillary plexus formed two groups, large peripheral venous radicles and sinusoidal medullary capillary plexus. Secondly, the medullary arteries supplied the inner cortex and medulla as true medullary capillary plexus. Therefore, the medullary capillary plexus composed of branches from cortical and medullary arteries. The medullary capillary plexus became a tributary of deep venous radicle. Both peripheral and deep venous radicles drained into the collecting, central, and adrenal veins, respectively. Furthermore, some medullary capillary plexus directly drained into the central vein without gathering into the collecting veins. Conclusions: Not only the microvascular connections in the cortex and medulla, but also several channels of the venous drainage were found in the glands of this animal model. Especially, the direct connections between the medullary capillary plexus and the central vein have not been demonstrated in other animal models. These direct routes may supply the sufficient blood to this organ, when the animal suddenly alters the positions. These findings also support the internal control of the cortex over the medulla. In addition, the pattern of adrenal microvascularization in this animal is similar to that in human. So that, this mammal is a suitable model for microvascular investigation.