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To revisit foetal development of the deep flexor tendons of the hand and foot, we examined the paraffin-embedded histology of 20 mid-term foetuses at 8–15 weeks of estimated gestational age (35–118 mm crown-rump length or CRL). At 8–9 weeks, in front of the metacarpal bones, the flexor pollicis longus and flexor digitorum profundus (FDP) muscles provided a plate-like, common tendon from which the lumbricalis muscles originated. However, in the foot, we had no evidence of such a common tendon. The flexor pollicis tendon was separated from the common tendon at 9–10 weeks possibly due to mechanical stress from the laterally growing thumb. Notably, at the lumbricalis muscle origins at 10–12 weeks, the FDP and flexor digitorum longus tendons remained undifferentiated and the primitive tenocytes were dispersed from them. The dispersed cells seemed to develop into an interface tissue between the lumbricalis muscle fibre and the deep tendon. In 3 of 5 specimens at 15 weeks, we found an excess number of the FDP tendons (5–7) in the proximal side of the lumbricalis muscle origin. However, the excess tendons dispersed in the lumbricalis muscle origin. The development of the lumbricalis muscle origin might follow the tendon splitting for four fingers. However, conversely, we hypothesised that the developing lumbricalis muscles re-arranged the deep flexor tendons to provide a configuration of “one deep tendon per one finger (or toe)”. The quadrates plantae muscle seemed not to contribute on the re-arrangement. (Folia Morphol 2012; 71, 3: 154–163)
Hypoxia is regarded as an important physiological factor that controls nephrogenesis. We investigated whether the renin-angiotensin-aldosterone system (RAAS) affects hypoxia-related target genes in developing kidneys. Newborn rat pups were treated with enalapril (30 mg/kg/d) or spironolactone (200 mg/kg/d) for 7 days. Tissue hypoxia was assessed by the uptake of a hypoxyprobe-1, pimonidazole (200 mg/kg), and the expression of hypoxia-responsive genes. In the enalapril group, hypoxia-inducible factor (HIF)-1, HIF-2, and Ets-1 protein expression were not changed, compared to the control group. In the spironolactone group, HIF-1 and Ets-1 protein expression were significantly increased by immunoblots and immunohistochemistry, whereas HIF-2 protein expression was not changed, compared to the control group. In the enalapril group, the immunoactivity of pimonidazole was not significantly different from that of the controls. However, in the spironolactone group, pimonidazole staining demonstrated that the cortex and medulla underwent severe hypoxia. In summary, our data showed that aldosterone inhibition in the developing kidney augmented the hypoxic responses, and up-regulated the expression of key mediators of hypoxia including HIF-1 and Ets-1. Angiotensin II inhibition did not affect hypoxia-related alterations in the developing kidney. The components of RAAS may differentially modulate renal hypoxia and its related target genes in the developing rat kidney.
Background: At birth, the ductus arteriosus (DA) merges with the aortic arch in the slightly caudal side of the origin of the left subclavian artery (SCA). Since the SCAs (7th segmental arteries) were fixed on the level of the 7th cervical-first thoracic vertebral bodies, the confluence of DA should migrate caudally. We aimed to describe timing and sequence of the topographical change using serial sagittal sections of 36 human embryos and foetuses (CRL 8–64 mm; 5–10 weeks), Those made easy evaluation of the vertebral levels possible in a few section. Materials and methods: The DA or 6th pharyngeal arch artery seemed to slide down in front of the sympathetic nerve trunk along 1.0–1.2 mm from the second cervical vertebral level at 5–6 weeks and, at 6 weeks (CRL 14–17 mm), the DA confluence with aorta reached the 7th cervical level. Because of the highly elongated common carotid artery, the sliding of DA confluence seemed to be much shorter than the cervical vertebrae growing from 1 mm to 2.4 mm. Results: At the final topographical change at 6–7 weeks, the DA confluence further descended to a site 1-vertebral length below the left SCA origin. From 6 to 9 weeks, a distance from the top of the aortic arch to the left SCA origin was almost stable: 0.3–0.5 mm at 6 weeks and 0.4–0.6 mm at 9 weeks. Conclusions: The heart descent and the caudal extension of the trachea and bronchi, those occurred before the DA sliding, were likely to be a major driving force for the sliding. (Folia Morphol 2019; 78, 4: 720–728)
Background: Prenatal twisting of the femoral neck seems to result in an angle of anteversion or torsion, but the underlying process has not been elucidated. Materials and methods: This study analysed sagittal, frontal and horizontal sections of 34 embryo and foetal specimens of gestational age (GA) 6–16 weeks (crown-rump length 21–130 mm). At GA 6–7 weeks, the iliopsoas (IP) and gluteus medius (GME) muscles were inserted into the anterior and posterior aspects of the femur, respectively, allowing both insertions to be viewed in a single sagittal section. Results: At GA 8 weeks, the greater trochanter and the femoral neck angle became evident, and the GME tendon was inserted into the upper tip of the trochanter. At GA 9 weeks, the location of IP insertion was to the medial side of the GME insertion. After 9 weeks, the IP insertion consisted of a wavy, tendinous part of the psoas muscle and another part of the iliacus muscle, with many fibres of the latter muscle attached to the joint capsule. After GA 12 weeks, the IP was inserted into the anteromedial side of the greater trochanter, while the aponeurotic insertion of the GME wrapped around the trochanter. At GA 15–16 weeks, a deep flexion at the hip joint caused an alteration in the relative heights of the lesser and greater trochanter, with the former migrating from the inferior to the slightly superior side. Conclusions: These findings indicate that twisting of the femoral neck started at GA 8–9 weeks. (Folia Morphol 2019; 78, 2: 408–418)
Ligament of Henle is one of muscle-associated connective tissues of the rectus abdominis muscle, but it has been confused with the conjoint tendon (a common aponeurosis for insertion of the inferomedial end of the obliquus internus and transversus abdominis muscles). To reconsider the inguinal connective tissue structures, we examined 20 mid-term foetuses (10 males and 10 females) at approximately 14–20 weeks of gestation (crown rump length 100–170 mm). In female horizontal sections, we consistently found the ligament of Henle as a wing-like aponeurosis extending from the lateral margin of the rectus tendon behind the superficial inguinal ring. The ligament was separated from and located behind the conjoint tendon. In all male foetuses, instead of the ligament, the conjoint tendon was evident behind the superficial ring and it winded around the posterior aspect of the spermatic cord. Therefore, although a limited number of specimens were examined, the ligament of Henle was likely to be a female-specific structure. The ligament of Henle, if developed well, may provide an arch-like structure suitable for a name “falx inguinalis” instead of the inferomedial end of the conjoint tendon. In addition, a covering fascia of the iliopsoas muscle joined the posterior wall of the inguinal canal in male, but not in female, specimens. (Folia Morphol 2013; 72; 2: 147–154)
Evaluation of semiserial sections of 14 normal hearts from human foetuses of gestational age 25–33 weeks showed that all of these hearts contained thin veins draining directly into the atria (maximum, 10 veins per heart). Of the 75 veins in these 14 hearts, 55 emptied into the right atrium and 20 into the left atrium. These veins were not accompanied by nerves, in contrast to tributaries of the great cardiac vein, and were negative for both smooth muscle actin (SMA) and CD34. However, the epithelium and venous wall of the anterior cardiac vein, the thickest of the direct draining veins, were strongly positive for SMA and CD34, respectively. In general, developing fibres in the vascular wall were positive for CD34, while the endothelium of the arteries and veins was strongly positive for the present DAKO antibody of SMA. The small cardiac vein, a thin but permanent tributary of the terminal portion of the great cardiac vein, was also positive for SMA and CD34. A few S100 protein-positive nerves were observed along both the anterior and small cardiac veins, but no nerves accompanied the direct drainage veins. These findings suggested that the latter did not develop from the early epicardiac vascular plexus but from a gulfing of the intratrabecular space or sinus of the atria. However, the immunoreactivity of the anterior cardiac vein suggests that it originated from the vascular plexus, similar to tributaries of the great cardiac vein. (Folia Morphol 2019; 78, 2: 283–289)
In the head and neck of human mid-term foetuses, the interface between areas of endochondral ossification and adjacent membranous (intramembranous) ossification is extensive. Using 8 foetal heads at 15–16 weeks, we have demonstrated differences in the matrices and composite cells between these 2 ossification processes, especially in the occipital squama and pterygoid process. Aggrecan-positive cartilage was shown to be invaded by a primitive bony matrix that was negative for aggrecan. At the interface, the periosteum was continuous with the perichondrium without any clear demarcation, but tenascin-c expression was restricted to the periosteum. In contrast, the interface between the epiphysis and shaft of the femur showed no clear localisation of tenascin-c. Versican expression tended to be restricted to the perichondrium. In the pterygoid process, the density of CD34-positive vessels was much higher in endochondral than in membranous ossification. The membranous part of the occipital was considered most likely to contribute to growth of the skull to accommodate the increased volume of the brain, while the membranous part of the pterygoid process seemed to be suitable for extreme flattening under pressure from the pterygoid muscles. (Folia Morphol 2014; 73, 2: 199–205)
Alzheimer's disease (AD) is characterized by deposition of β-amyloid (Aβ) in areas of the brain. Aβ is a metabolic fragment of the β-amyloid precursor protein (βAPP). Genetic evidence has linked βAPP to AD, and there is increasing evidence that fragments from βAPP are neurotoxic. Aβ, the main research focus, has been shown to induce depolarizing ion channel activity. Involvement of other cleaved products from βAPP are less clear. We have investigated the 105 amino acid C-terminal peptide (CT105) (containing the full sequence Aβ), an alternative fragment linked with cellular toxicity. CT105 induced non-selective ionic currents in Xenopus oocytes (a model cell used in cell signalling studies) and was toxic to oocytes and mammalian cortical neurones. These results suggest possible involvement of CT105 in inducing the neural toxicity characteristic of AD.
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