The aim of this study was to evaluate the features of pulmonary histopathological changes in cases of trisomy 18 complicated with congenital heart disease and pulmonary arterial hypertension. Twenty‐eight patients with trisomy 18 underwent open lung biopsy at the time of primary operation in our hospital between 2008 and 2019. We compared these histopathological findings with those from previously described groups without trisomy 18. Mean age at primary cardiac surgery was 37 days (range, 9–69 days). According to the Heath‐Edwards (HE) classification, 1, 8, 12, and 5 patients were graded as 0, 1, 2, and 3, respectively, whereas 2 patients were not classifiable due to medial defects in the small pulmonary arteries (MD). Four (14.3%) and 13 (46.4%) patients presented with MD and hypoplasia of the small pulmonary arteries (HS). Fifteen (53.6%) and 21 (75.0%) patients presented with alveolar hypoplasia (AH) and alveolar wall thickening (AT). MD, HS, and AH in trisomy 18 were present frequently, differing significantly from previous reports. These findings might be associated with congenital inadequate development of vessels and alveoli in the lung, contributing to a high risk of PAH in trisomy 18.

ABSTRACT. We evaluated transcervical insemination (TCI) using frozen semen by flexible endoscopy in dogs. Eight female and eight male beagles were used in this study. A flexible endoscope and a washing tube were used for TCI. A tracheal tube was used as an alternative to the penis and was an auxiliary for inserting the flexible endoscope. The mean time required to insert the washing tube into the external os of the uterus after inserting the endoscope into the tracheal tube was 7.5 min. Slight or mild pain was observed in all bitches during TCI. However, TCI could be easily performed with retention in all bitches and without sedation anesthesia. The tracheal tube was useful to ensure the visual field using air sufflation. Clinical signs suspicious of infection were not observed in any bitches from the TCI to the pregnancy diagnosis. The conception rate was 87.5%, and the mean number of fetuses was 6.3. TCI using a flexible endoscope in bitches was performed quickly with minimal invasiveness. We present a new method of TCI in dogs. This method should be studied in small and large breeds to obtain more detailed results. Artificial insemination (AI) using frozen semen in dogs has been increasing in recent years. However, AI using cryopreserved semen generally yields lower pregnancy rates with vaginal deposition than with uterine deposition because of the short life span of frozen-thawed spermatozoa [5,19]. Therefore, AI methods usually use uterine deposition with frozen semen. Surgical insemination is highly invasive and requires general anesthesia, whereas transcervical insemination (TCI) using metal catheterization is minimally invasive but requires a skilled technique [24]. In contrast, TCI using a rigid endoscope is easy and less invasive [13,30]. TCI with a flexible endoscope is also less invasive because the scope is soft, and it has an air supply and instrument channel, which endows it with good operability [21,29]. Therefore, a flexible endoscope might be useful as a new tool for TCI.The purpose of this study was to evaluate TCI using frozen semen by flexible endoscope in dogs. MATERIALS AND METHODSEight female beagles aged 1-8 years (mean ± standard deviation: SD, 4.1 ± 2.5 years) and weighing 10.7-15.1 kg (mean ± SD, 12.8 ± 1.3 kg) were used in this study; 4 were parous, and the others were nulliparous. Eight male beagles aged 1-7 years (mean ± SD, 3.6 ± 1.8 years) and weighing 11.4-15.8 kg (mean ± SD, 13.1 ± 1.4 kg) were used as sperm donors. Unrelated dogs were used to prevent inbreeding. This study was performed in accordance with the Guide for the Experimentation of Animals of the College of Bioresource Sciences, Nihon University (AP11B018, 2010).The sperm-rich fraction of a single ejaculate was collected from each dog by digital manipulation [11]. The collected semen was centrifuged at 400 × g for 5 min. The supernatant was discarded, and the pellets were gently suspended in 1 ml with egg-yolk Tris-fructose citrate extender supplemented with 1% Orvus ES paste (OEP) [26][27][28]. Sperm concentration w...

We present a case of a healthy 7-month-old female infant who developed sudden le heart failure due to acute mitral regurgitation (MR). She was rushed to our hospital on the day of onset and underwent semiemergency surgery the next day. Antimicrobial treatment was initiated upon admission, and pyrexia occurred 8 h later. At surgery, the anatomical ndings included the destruction of both the anterior and posterior lea ets of the mitral valve, posterior mitral valve lea et perforation, an undetected rupture of the chordae tendineae, and no vegetation on the mitral valve. Mitral valve replacement was performed because of the di culty of mitral valve annuloplasty. A culture test of blood and resected anterior mitral valve demonstrated no bacterial or fungal infection, but histopathological analysis revealed polymorphonuclear cell in ltration of the resected mitral valve lea et.e patient was diagnosed with infective endocarditis (IE) based on these ndings; however, we were unable to determine the cause of infection or pathogenic bacteria. Acute MR in infants can be caused by IE and acute rupture of the chordae tendineae of the mitral valve (RCTMV). e current case of infantile IE started with acute MR due to signi cant valvular destruction, followed by pyrexia, and progressed quickly, similar to RCTMV in infants. Because the treatment and complications of acute MR in healthy infants are dependent on the cause, we must take special care to ascertain the cause along with histopathological analysis.Keywords: acute mitral regurgitation, infective endocarditis, mitral valve perforation, acute rupture of the chordae tendineae of the mitral valve in infants

Pulmonary veno-occlusive disease (PVOD) is a rare condition that results in pulmonary hypertension caused by the occlusion of the peripheral pulmonary veins. A 1-month old infant with patent ductus arteriosus presented in critical condition with pulmonary hypertensive crisis. Cardiac catheterization revealed severe pulmonary hypertension (pulmonary to systemic arterial pressure ratio, 1.3; mean pulmonary arterial pressure, 43 mmHg; pulmonary wedge pressure, 6 mmHg; pulmonary vascular resistance, 10.3 units•m 2 ). e patient was started on combination therapy, including continuous intravenous epoprostenol. Although drugs targeting pulmonary arterial hypertension (PAH) were initially able to improve his hemodynamic status, he gradually developed pulmonary edema. Histopathological nding of lung biopsy specimen showed PAH, so he was diagnosed with idiopathic PAH. However, he experienced recurrent pulmonary edema and progressive right heart failure. One year a er admission, the patient died from severe heart failure. Histopathological autopsy ndings of the lung showed pulmonary venous changes and intimal thickening of the pulmonary veins, and a diagnosis of PVOD was made. Pulmonary arterial changes included cellular and brous thickening of the intima, severe medial hypertrophy, and adventitial thickening with plexiform lesions (Heath Edwards grade 4). A correct diagnosis in this case could not be made by single lung biopsy. Our experience suggests that we should suspect PVOD when patients receiving PAH therapy develop recurrent pulmonary edema, as the only available method of PVOD treatment is early lung transplantation.