Failure Of Fusion Research Articles

A collapse risk assessment method for subway foundation pit based on cloud model and improved Dempster–Shafer evidence theory

Collapse is a major engineering hazard in open-cut foundation pit construction, and risk assessment is crucial for considerably reducing engineering hazards. This study aims to address the ambiguity problem of qualitative index quantification and the failure of high-conflict evidence fusion in risk assessment. Thus, a fast-converging and high-reliability multi-source data fusion method based on the cloud model (CM) and improved Dempster–Shafer evidence theory is proposed. The method can achieve an accurate assessment of subway pit collapse risks. First, the CM is introduced to quantify the qualitative metrics. Then, a new correction parameter is defined for improving the conflicts among evidence bodies based on conflict degree, discrepancy degree and uncertainty, while a fine-tuning term is added to reduce the subjective effect of global focal element assignment. Finally, the risk assessment result is obtained according to the maximum affiliation principle. The method is successfully applied to Luochongwei Station, where the difference between the maximum value and the second largest value of the basic probability assignment is 0.624, and the global uncertainty degree is 0.087. Both values satisfy the decision evaluation condition; however, values of other methods only satisfy one or neither condition. In addition, the proposed method requires only four cycles to reach the steady state by fusing data of the same index, which has faster convergence compared with that of other methods. The proposed method has good universality and effectiveness in subway pit collapse risk assessment.

Failure mode division and remaining useful life prognostics of multi-indicator systems with multi-fault

Modern large-scale industrial systems are complex in structure, and their health states are usually reflected by multiple indicators. The performance degradation of multiple indicators surpasses respective threshold, causing multiple system faults, and multiple failure modes such as redundancy, fusion, and competition among different fault combinations exist, introducing new challenges when predicting remaining useful life (RUL) of the system. This study aims to establish a unified multi-failure mode division framework and the RUL prediction model under different failure modes for multi-indicator systems. Firstly, combination relationship between different fault types caused by multi-indicators outweighing their threshold is analyzed, and different redundancy, fusion, and competition failure modes are defined. Next, the formal fault type definition and its remaining time before occurrence under different failure modes are provided. The distribution calculation model of remaining time for different fault types is derived. The corresponding system's RUL prediction model under multi-fault competition is established, and degradation modeling, parameter estimation, and RUL distribution calculation are performed using the state-space model. Eventually, the validity of the RUL prediction model according to multiple failure modes is verified by numerical experiments. Taking XJTU-SY bearing and C-MAPSS datasets as two examples, the applicability and feasibility of the given method are proved.

Risk factors affecting spinal fusion: A meta-analysis of 39 cohort studies.

We performed a meta-analysis to identify risk factors affecting spinal fusion. We systematically searched PubMed, Embase, and the Cochrane Library from inception to January 6, 2023, for articles that report risk factors affecting spinal fusion. The pooled odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using fixed-effects models for each factor for which the interstudy heterogeneity I2 was < 50%, while random-effects models were used when the interstudy heterogeneity I2 was ≥ 50%. Using sample size, Egger's P value, and heterogeneity across studies as criteria, we categorized the quality of evidence from observational studies as high-quality (Class I), moderate-quality (Class II or III), or low-quality (Class IV). Furthermore, the trim-and-fill procedure and leave-one-out protocol were conducted to investigate potential sources of heterogeneity and verify result stability. Of the 1,257 citations screened, 39 unique cohort studies comprising 7,145 patients were included in the data synthesis. High-quality (Class I) evidence showed that patients with a smoking habit (OR, 1.57; 95% CI, 1.11 to 2.21) and without the use of bone morphogenetic protein-2 (BMP-2) (OR, 4.42; 95% CI, 3.33 to 5.86) were at higher risk for fusion failure. Moderate-quality (Class II or III) evidence showed that fusion failure was significantly associated with vitamin D deficiency (OR, 2.46; 95% CI, 1.24 to 4.90), diabetes (OR, 3.42; 95% CI, 1.59 to 7.36), allograft (OR, 1.82; 95% CI, 1.11 to 2.96), conventional pedicle screw (CPS) fixation (OR, 4.77; 95% CI, 2.23 to 10.20) and posterolateral fusion (OR, 3.63; 95% CI, 1.25 to 10.49). Conspicuous risk factors affecting spinal fusion include three patient-related risk factors (smoking, vitamin D deficiency, and diabetes) and four surgery-related risk factors (without the use of BMP-2, allograft, CPS fixation, and posterolateral fusion). These findings may help clinicians strengthen awareness for early intervention in patients at high risk of developing fusion failure.

Myelomeningocele: Long-Term Neurosurgical Management.

Open spina bifida, also known as myelomeningocele (MMC), is the most challenging and severe birth defect of the central nervous system compatible with life and it is due to a failure in the dorsal fusion of the nascent neural tube during embryonic development. MMC is often accompanied by a constellation of collateral conditions, including hydrocephalus, Arnold - Chiari II malformation, brainstem disfunction, hydrosyringomyelia, tethered cord syndrome and scoliosis. Beyond early surgical repair of the dorsal defect, MMC requires lifelong cares. Several additional surgical procedures are generally necessary to improve the long-term outcomes of patients affected by MMC and multidisciplinary evaluations are crucial for early identification and management of the various medical condition that can accompany this pathology. In this chapter, the most common pathological entities associated with MMC are illustrated, focusing on clinical manifestations, treatment strategies and follow up recommendations.

A Complete Non-fusion of Sacral Spines- a Rare Anomaly: A Case Report

Background: Human sacrum is a large triangular bone formed by fusion of five separate sacral vertebrae and their intervertebral disc. The dorsal surface of sacrum presents triangular sacral canal formed by fusion of sacral vertebral foramina. The opening present at the caudal end of the sacral canal is known as sacral hiatus. Sacral hiatus is formed due to failure of fusion of lamina and spinous process of fifth or fourth sacral vertebrae. Spina bifida occulta is a condition resulting due to incomplete fusion of neural arch of vertebrae, mainly in lumbosacral region. When the condition of spina bifida occulta occurs in the sacrum, the level of non-closure becomes variable. Materials and Methods: A dry human sacrum with full agenesis of the dorsal wall of the sacral canal was identified during regular osteology demonstration lessons for undergraduate BAMS students at Department of Sharir Rachana (Anatomy), Ayurveda Campus, Institute of Medicine, Tribhuvan University, Kathmandu, Nepal. Non-metric differences in spines were thoroughly examined. Results and Discussion: Spina bifida is the generic term for range of discrete defects of neurulation and subsequent vertebral formation. The various forms of neural tube and vertebral defects have been reported such as craniorachisis, anencephaly and myocele. In this case a spine with complete sacral spina bifida occulta was discovered. The posterior laminae of all sacral vertebrae were completely unfused in this specimen. It's more likely that the sacral region was a groove than a canal. There were no additional abnormalities discovered. Many studies on incidence of spina bifida occulta have been published with mixed results. The frequency reported by researchers and population varies substantially. Conclusion: The complete agenesis of the dorsal wall of the sacral canal in these variants is critical for diagnosing lower back pain, sciatica, and caudal regression syndrome, as well as avoiding problems from caudal epidural block and other spinal procedures, such as screw placement for spinal fusion.

A novel porous interbody fusion cage modified by microarc oxidation and hydrothermal treatment technology accelerate osseointegration and spinal fusion in sheep.

The clinical outcome of spinal fusion surgery is closely related to the success of bone fusion. Nowadays, the interbody cage which is used to replace the disc for spinal fusion is expected to have biological activity to improve osseointegration, especially for the aging and osteoporotic patients. Here, through micro-arc oxidation and hydrothermal treatment (MAO + HT), a bioactive CaP coating with micro/nano multilevel morphology was developed on 3D printed Ti6Al4V alloy then verified in vitro and in sheep anterior cervical decompression fusion model systematically. In vitro studies have confirmed the positive effects of characteristic micro/nano morphology and hydrophilicity of the coating formed after surface treatment on the adhesion, proliferation, and osteogenic differentiation of osteoblast precursor cells. Furthermore, the MAO + HT treated interbody cage showed a closer integration with the surrounding bone tissue, improved kinetic stability of the implanted segment, and significantly reduced incidence of fusion failure during the early postoperative period, which indicated that such a surface modification strategy is applicable to the biomechanical and biological microenvironment of the intervertebral space.

Claudin-3 in the non-neural ectoderm is essential for neural fold fusion in chicken embryos

The neural tube, the embryonic precursor to the brain and spinal cord, begins as a flat sheet of epithelial cells, divided into non-neural and neural ectoderm. Proper neural tube closure requires that the edges of the neural ectoderm, the neural folds, to elevate upwards and fuse along the dorsal midline of the embryo. We have previously shown that members of the claudin protein family are required for the early phases of chick neural tube closure. Claudins are transmembrane proteins, localized in apical tight junctions within epithelial cells where they are essential for regulation of paracellular permeability, strongly involved in apical-basal polarity, cell-cell adhesion, and bridging the tight junction to cytoplasmic proteins. Here we explored the role of Claudin-3 (Cldn3), which is specifically expressed in the non-neural ectoderm. We discovered that depletion of Cldn3 causes folic acid-insensitive primarily spinal neural tube defects due to a failure in neural fold fusion. Apical cell surface morphology of Cldn3-depleted non-neural ectodermal cells exhibited increased membrane blebbing and smaller apical surfaces. Although apical-basal polarity was retained, we observed altered Par3 and Pals1 protein localization patterns within the apical domain of the non-neural ectodermal cells in Cldn3-depleted embryos. Furthermore, F-actin signal was reduced at apical junctions. Our data presents a model of spina bifida, and the role that Cldn3 is playing in regulating essential apical cell processes in the non-neural ectoderm required for neural fold fusion.

Presurgical orthopedics in patient with cleft lip and palate without cheiloplasty at one year of age.

Introduction. Cleft lip/palate (CLP) occurs due to failure of fusion of facial processes at an early stage of embryonic development. The use of pre-surgical orthopedics helps us to correct the bone collapse that patients with CLP may present, as well as stimulate the growth of the palatal segments, with use beginning in the first hours of life. Due to the pandemic caused by COVID, many patients did not receive care, generating a need for treatment focused on their characteristics. Aim. Generate transversal development in a 1-year-old male patient and rotate the left maxillary segment to conform the arch, and thus, favor the prognosis of surgery for the patient with cleft lip and palate without cheiloplasty at one year of life. Description of the case. Male patient with cleft lip and palate without cheiloplasty at one year of age presents to cleft lip and palate clinic YOU HAVE TO SMILE, JOIN EFFORTS. He refers to having been treated with pre-surgical orthopedics. Clinically, a cleft lip and palate is observed, in addition to the collapsed left maxillary segment, generating a lack of continuity and arch perimeter. The treatment phase consisted of a removable plate joined in its central part by three helixes, to rotate the left maxillary segment. Results. An adequate maxillary development was generated and the arch was shaped. conclusions. It is important to highlight the characteristics of each case in order to generate a treatment plan suitable for the needs of the patient, since this improves the prognosis and post-surgery.

Buckling Mechanism Simulation for Thin-Wall Components Made by Laser Powder Bed Fusion

The effect of part geometry on premature thin wall part failure in laser powder bed fusion (LPBF) is investigated using FEM simulation. Two FEM models are used to simulate the residual stress and buckling modes. Two experimental parts with different lengths are used for model validations. A LPBF FEM model evaluates the residual stress associated with the two experimental parts. A parametric buckling model is developed to determine the eigenvalues for 100 different part geometries including different part lengths (20-60 mm), widths (0.5-2 mm), and heights (10-50 mm). The results show that thin wall parts are more susceptible to buckling mode 1 when part length is small and to a combination of mode 1 and 3 when part length increases. In both cases the threshold stress for buckling is mostly sensitive to part thickness and height.

Multipartite patella: A review of diagnostic techniques and management of the symptomatic patient.

Multipartite patella is an anatomical variant classified by the fragmentation of the main patellar body. The cause of this variant is due to failure in fusion of the patellar ossification centers. It is commonly misdiagnosed as a fracture of the patella in clinical practice, leading to unnecessary treatment measures. The aim of this review is to provide an overview of the development and classification of this variation, diagnostic imaging techniques, and assess the optimal management technique for the symptomatic patient. Multiple radiographic methods are used to identify this variant, with recent studies highlighting high sensitivity rates for nonradiative methods (ultrasound). In terms of symptomatic management, accessory fragment excision and vastus lateralis release provide the greatest alleviation of symptoms, with screw fixation being less favorable.

Pregnancy with uterine didelphys and history of recurrent pregnancy loss: Case report

Link of Video Abstract: https://youtu.be/H7Y7XoPOUAw Background: Uterine didelphys is an embryologic disorder that arises from the failure of Mullerian duct fusion. It is characterized by the presence of two distinct cervices, two vaginas, and two uterine horns. Obstetric complications may arise during pregnancy when uterine didelphys is present; these may include spontaneous abortion, premature labour, and fetal malpresentation. Case Presentation: A 25-year-old woman has been married for three years and had history of six gravid, zero parity, and five abortion. The patient had uterine didelphys. A fully septated uterus with double cervices and vaginas was found on pelvic magnetic resonance imaging. The patient arrived at the hospital at 27/28 weeks. Periodic sonograms demonstrated breech presentation and no (Intrauterine Growth Restriction) IUGR evidence. At 38/39 weeks, the patient was scheduled for cesarean surgery. Uterine didelphys morphology, pregnancy on the left side of the uterus, and the septum separating the left and right uterine cavities were all observed during the caesarean section. The newborn had three umbilical cords wrapped around his neck. The infant was female, 2800 grams, 48 cm, Apgar score 7-8, Ballard score (BS) 38 weeks, Lubchenco score (LS) p25-50. Conclusion: Antenatal care is required for investigating risks of uterine didelphys, including cervical incompetence, spontaneous abortion, and preterm birth, using serial sonograms to assess fetal well-being and cervical length.

Inhibition of PDGFRβ alleviates endothelial cell apoptotic injury caused by DRP-1 overexpression and mitochondria fusion failure after mitophagy

Kawasaki disease (KD), described as “mucocutaneous lymph node syndrome”, affects infants and toddlers. Patients with KD suffer from an inflammatory cascade leading to vasculitis with a predilection for coronary arteries. While the symptoms and pathogenesis of KD have received more and more attention, the precise mechanisms are still debated. Researches show that endothelial dysfunction process in KD leads to arterial damage and affect clinical outcome. In this study, we constructed a Candida albicans water soluble fraction (CAWS)-induced KD murine model and penetrated investigating the mechanisms behind endothelial dysfunction. CAWS-induced mice presented remarkably elevated vascular endothelial cell growth factor (VEGF) levels. Abundant expression of VEGF was documented in all vessels that showed edema from acute KD. It has been reported that Platelet-derived growth factor (PDGF) co-expression normalizes VEGF-induced aberrant angiogenesis. Hyperexpression of PDGFRβ was induced in the thickened medial layer and vascular endothelium of KD mice. Masitinib (Mas) is an oral tyrosine kinase inhibitor of numerous targets, which can selectively target PDGFR signaling. We set out to explore whether Mas could regulate coronary pathology in KD. Mas administration significantly reduced the VEGF-induced endothelial cells migration. NOX4 was activated in vascular endothelial cells to produce more ROS. Mitochondrial dysregulated fission and mitophagy caused by DRP-1 overexpression precipitated the arterial endothelial cells injury. Here, mitophagy seemed to work as the driving force of DRP-1/Bak/BNIP3-dependent endothelial cells apoptosis. In summary, how mitophagy is regulated by DRP-1 under pathologic status is critical and complex, which may contribute to the development of specific therapeutic interventions in cardiovascular diseases patients, for example Masatinib, the inhibitor of PDGFRβ.Facts and questionsKawasaki disease causing systemic vasculitis, affects infants and toddlers.Coronary artery injury remains the major causes of morbidity and mortality.DRP-1 overexpression induces DRP-1/Bak/BNIP3-dependent endothelial cells apoptosis.PDGFRβ was high-expressed in the thickened medial layer of CAWS-induced KD mice.Inhibition of PDGFRβ signaling alleviates arterial endothelial cells injury.

THE PREVALENCE AND PROFILE OF AFRICAN PATIENTS WITH OS ACROMIALE THAT PRESENT WITH SHOULDER PAIN AT A TERTIARY HOSPITAL IN PRETORIA, SOUTH AFRICA

Os acromiale is a developmental defect caused by failure of fusion of the anterior epiphysis of the acromion between the ages of 22 and 25. The prevalence of os acromiale in the general population ranges from 1.4% to 15%. Os acromiale has been reported as a contributory factor to shoulder impingement symptoms and rotator cuff injuries, despite being a common incidental observation. In this retrospective study, we examined the prevalence of os acromiale in black African patients with shoulder pain.We retrospectively reviewed the clinical records, radiographs, and magnetic resonance imaging (MRI) scans of 119 patients who presented with atraumatic and minor traumatic shoulder pain at a single institution over a one-year period. Anteroposterior, scapula Y-view, and axillary view plain images were initially evaluated for the presence of os acromiale, and this was corroborated with axial MRI image findings. Patients with verified os acromiale had their medical records reviewed to determine their first complaint and the results of their clinical examination and imaging examination.Radiographs and MRI on 24 patients (20%) revealed an osacromiale. This cohort had a mean age of 59.2 years, and there were significantly more females (65%) than males. Meso-acromion was identified as the most prevalent type (n=11), followed by pre-os acromion (n=7). All patients underwent bilateral shoulder x-rays, and 45 percent of patients were found to have bilateral meso- acromion. Most patients (70%) were reported to have unstable os acromiale with subacromial impingement symptoms, and nine patients (36%) had confirmed rotator cuff tears based on clinical and Mri findings. Surgery was necessary for 47% of the 24 patients with confirmed Os acromiale (arthroscopic surgery, n=7; open surgery, n=1) in order to treat their symptomsThe prevalence of os acromiale in our African patients with atraumatic shoulder symptoms is greater than that reported in the general population. Os acromiale is a rare condition that should always be considered when evaluating shoulder pain patients.

Abstract 12877: Giant Pericardial Cyst Causing Syncope

A 30 year old male presented with episodes of near syncope with dizziness, palpitations, chest tightness, and left arm paresthesias. Upon presentation, his vitals were normal. Initial imaging of a chest radiograph showed an enlarged cardiac silhouette and a follow-up chest CT demonstrated a 10 cm cystic mass in the anterior mediastinum concerning for a giant pericardial cyst. Echocardiogram was performed which showed a normal ejection fraction, no valvular abnormalities, and a trivial pericardial effusion. A CT-guided drainage was performed with 440mL of fluid removed and shrinkage of the cyst to 27x63mm. The aspirate was loaded with leukocytes without organisms identified. The following day, the cyst recollected to 85x69mm. Repeat CT-guided drainage was attempted however was unsuccessful due to right pneumothorax. After resolution of the pneumothorax, he was asymptomatic prompting discharge with close outpatient follow-up. Outpatient imaging demonstrated increased size of the pericardial cyst to 11 cm in diameter. A third drainage via CT-guidance was attempted however only minimal fluid was able to be drained. As the patient remained asymptomatic, it was recommended the patient have repeat imaging in 6 months and monitor for symptoms. Pericardial cysts are relatively rare and comprise 7% of mediastinal masses. They originate from failed fusion of the mesenchymal lacunae that form the pericardial coelom. Pericardial cysts typically range from 1 to 5 cm in diameter, with those over 10cm being termed 'giant pericardial cysts'. Most cysts are asymptomatic, although if symptoms do occur they are generally in response to mass effect and compression of local structures, such as shortness of breath and chest discomfort. If a patient remains asymptomatic, conservative management with serial imaging is recommended. However, if a patient becomes symptomatic or develops complications, surgical management via a pericardectomy or percutaneous aspiration is recommended.

Whole Exome Sequencing Identifies Damaging Variants in Indonesians with Clefts.

The interaction between genomics, genetic and environmental factors have been implicated in non-syndromic orofacial cleft development. In the current study, we investigated the contributions of rare and novel genetic variants in known cleft genes using whole exome sequencing (WES) data of Indonesians with non-syndromic orofacial clefts. WES was conducted on 6 individuals. Variants in their exons were called and annotated. These variants were filtered for novelty and rarity using MAF of 0 and 1%. Hospital in Indonesia. Indonesians with non-syndromic orofacial clefts. Deleterious variants were prioritized. Pathogenic amino acid changes effect on protein structure and function were identified using HOPE. Rare and novel variants in known cleft genes were filtered and their deleteriousness were predicted using polyphen, SIFT and CADD. We identified rare (MAF <1%) deleterious variants in 4 craniofacial genes namely MMACHC (rs371937044, MAF = 0.00011). SOS1 (rs190222208, MAF = 0.00045), TULP4 (rs199583035, MAF = 0.067), and MTHFD1L (rs143492706, MAF = 0.0044). MMACHC has a mouse knockout model with facial cleft and failure of palatal fusion. The individual with variant in MMACHC presented with nsCPO. Our study provides additional evidence for the role of TULP4, SOS1, MTHFD1L and MMACHC genes in nsOFC development. This is the first time MMACHC is implicated in nsOFC development in humans.

Cell adhesion marker expression dynamics during fusion of the optic fissure

Tissue fusion is a critical process that is repeated in multiple contexts during embryonic development and shares common attributes to processes such as wound healing and metastasis. Ocular coloboma is a developmental eye disorder that presents as a physical gap in the ventral eye, and is a major cause of childhood blindness. Coloboma results from fusion failure between opposing ventral retinal epithelia, but there are major knowledge gaps in our understanding of this process at the molecular and cell behavioural levels. Here we catalogue the expression of cell adhesion proteins: N-cadherin, E-cadherin, R-cadherin, ZO-1, and the EMT transcriptional activator and cadherin regulator SNAI2, in the developing chicken embryonic eye. We find that fusion pioneer cells at the edges of the fusing optic fissure have unique and dynamic expression profiles for N-cad, E-cad and ZO-1, and that these are temporally preceded by expression of SNAI2. This highlights the unique properties of these cells and indicates that regulation of cell adhesion factors may be a critical process in optic fissure closure.

The roles of JAK2/STAT3 signaling in fusion of the secondary palate.

Cleft palate has a multifactorial etiology. In palatal fusion, the contacting medial edge epithelium (MEE) forms the epithelial seam, which is subsequently removed with the reduction of p63. Failure in this process results in a cleft palate. We herein report the involvement of janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling in palatal fusion and that folic acid rescues the fusing defect by reactivating JAK2/STAT3. In closure of bilateral palatal shelves, STAT3 phosphorylation was activated at the fusing MEE and mesenchyme underlying the MEE. JAK2 inhibition by AG490 inhibited STAT3 phosphorylation and resulted in palatal fusion failure without removal of the epithelial seam, in which p63 and keratin 17 (K17) periderm markers were retained. Folic acid application restored STAT3 phosphorylation in AG490-treated palatal explants and rescued the fusion defect, in which the p63- and K17-positive epithelial seam were removed. The AG490-induced palatal defect was also rescued in p63 haploinsufficient explants. These findings suggest that JAK2/STAT3 signaling is involved in palatal fusion by suppressing p63 expression in MEE and that folate restores the fusion defect by reactivating JAK2/STAT3.

Tailoring Fusion-Based Error Correction for High Thresholds to Biased Fusion Failures.

We introduce fault-tolerant (FT) architectures for error correction with the XZZX cluster state based on performing measurements of two-qubit Pauli operators Z⊗Z and X⊗X, or fusions, on a collection of few-body entangled resource states. Our construction is tailored to effectively correct noise that predominantly causes faulty X⊗X measurements during fusions. This feature offers a practical advantage in linear optical quantum computing with dual-rail photonic qubits, where failed fusions only erase X⊗X measurement outcomes. By applying our construction to this platform, we find a record-high threshold to fusion failures exceeding 25% in the experimentally relevant regime of nonzero loss rate per photon, considerably simplifying hardware requirements.

A possible manifestation of pancreas divisum–pancreatic pseudocyst in an infant with no apparent history of pancreatitis: a case report

BackgroundPancreas divisum (PD), the most common pancreatic anomaly, is caused by the failure of pancreatic bud fusion in the embryo. Although most cases are asymptomatic, it can cause pancreatitis or epigastric pain. We report an unusual case of PD in an infant.Case presentationThe patient was a 9-month-old girl with no pertinent medical history. She had suffered vomiting and diarrhea for 1 week before transfer to our hospital. Her general condition was poor, and abdominal distention was noted. Blood tests revealed microcytic anemia with normal chemical markers. The parents reported no episode of pancreatitis. Ultrasonography revealed massive ascites, which was later found to be bloody. Enhanced computed tomography and magnetic resonance imaging depicted a cystic lesion, approximately 2 cm in size, anterior to the second portion of the duodenum. During exploratory laparotomy, a pinhole was identified on the cyst wall, which was mistakenly identified as a duodenal perforation, and direct closure was performed. Postoperative levels of serum amylase and inflammation markers were elevated, and the amount of ascites increased, impairing oral feeding. The level of pancreatic enzymes in the ascites was high. Imaging studies were repeated, but the cause of pancreatic fistula was not identified. Conservative therapy, including administration of total parenteral nutrition, antibiotics, and octreotide, was initiated, but the situation did not improve. Three months after admission, endoscopic retrograde cholangiopancreatography showed a thick dorsal pancreatic duct communicating with a hypoplastic ventral duct, which was indicative of PD. Contrast medium leaking from the dorsal duct near the minor ampulla revealed the presence of a pseudocyst. Stenting via the minor papilla was impossible because the minor papilla was obstructed. Instead, a stent was inserted into the ventral pancreatic duct. Endoscopic transgastric drainage of the cyst was effective, and the patient was discharged, 7 months after admission. The patient is healthy, but the gastric stent needs to be replaced regularly.ConclusionIn children, PD can manifest with pancreatic pseudocyst that causes pancreatic ascites, even in the absence of pancreatitis. This may be a previously unrecognized manifestation of PD in children, and clinicians need to be aware of it.

Ventricular septal defect in octogenarian: a case report

It is not a common case that we see in our day-to-day clinical practice, a patient presenting with congenital VSD at the age of eighty. Ventricular septal defect (VSD) is a developmental defect of the interventricular septum resulting from a deficiency of growth or a failure of alignment or fusion of component parts of ventricular septum.1Ventricular septal defects are the most common form of congenital heart disease and among the most frequently seen congenital abnormalities.2Perimembranous defects are the most common types of ventricular septal defects and account for 80% of such defects.3It is estimated that 25–40% of VSDs will close by the age of 2 years, and they are unlikely to persist after the age of 10 years; thus adults with congenital heart disease, VSDs represent only about 10% of the cases.4