Explore the vast range of titles available.

Background An atrial septal defect (ASD) is considered oval-shaped when its shortest diameter is less than 75% of the longest diameter. Research on percutaneous closure of oval-shaped ASDs is limited, with no known reports of non-fluoroscopic closure for this population. Objective To assess the effectiveness of non-fluoroscopic percutaneous closure for oval-shaped ASDs. Methods This single-center retrospective study evaluates patients undergoing non-fluoroscopic percutaneous closure of oval-shaped ASDs, defined by the shortest to longest diameter ratio < 0.75, a circular index of 1.33, or ultrasound visualization of an oval shape. Device size was chosen to be 0–4 mm larger than the defect’s longest diameter, based on transthoracic and transesophageal ultrasound measurements. Results We identified 78 patients (33.3% children, 20.5% males) with a mean age of 27.4 ± 16.3 years and a mean weight of 46.8 ± 19.8 kg. The mean longest diameter and mean shortest diameter of ASDs were 23.3 ± 6.8 mm and 15.8 ± 5 mm, respectively. The mean ratio of the shortest to longest diameter was 0.7 ± 0.1. Percutaneous closure was not attempted in 7/78 (9%) patients. Three out of 71 (4.2%) procedures were fluoroscopy-guided upfront due to technical difficulties, and 5/71 (7%) were converted to fluoroscopy-guided closure. Overall procedural success rate was 98.6% (70/71) including 63/71 (88.7%) performed with zero fluoroscopy. Mean device size was 26.5 ± 7.1 mm. Mean procedural time was 45.3 ± 22.6 min. Eleven intraprocedural complications occurred including 6 arrhythmias, 3 pericardial effusions, and 2 device dislodgements. Conclusion Transcatheter closure of oval-shaped ASD is safe and feasible. Echocardiography is adequate for adequate operative guidance.

ABSTRACT Berry syndrome is an extremely rare constellation of several congenital cardiac anomalies consisting of aortopulmonary window, aortic origin of the right pulmonary artery (AORPA), interrupted aortic arch or hypoplastic aortic arch or coarctation of the aorta, and an intact ventricular septum with high neonatal mortality rates. The disease is fatal with high mortality (90%) in the neonatal period with surviving patients mostly developing pulmonary hypertension. We describe the clinical presentation and diagnostic clues in two patients with Berry syndrome.

Fragile X syndrome is caused by a loss of expression of the fragile X mental retardation protein (FMRP). FMRP is a selective RNA-binding protein which forms a messenger ribonucleoprotein (mRNP) complex that associates with polyribosomes. Recently, mRNA ligands associated with FMRP have been identified. However, the mechanism by which FMRP regulates the translation of its mRNA ligands remains unclear. MicroRNAs are small noncoding RNAs involved in translational control. Here we show that in vivo mammalian FMRP interacts with microRNAs and the components of the microRNA pathways including Dicer and the mammalian ortholog of Argonaute 1 (AGO1). Using two different Drosophila melanogaster models, we show that AGO1 is critical for FMRP function in neural development and synaptogenesis. Our results suggest that FMRP may regulate neuronal translation via microRNAs and links microRNAs with human disease.

Reports of synchronous spawning in corals of Lakshadweep reefs, India have been purely anecdotal. To understand factors that underlie coral spawning in Lakshadweep, we studied four Acropora species (A. muricata, A. cytherea, A. hemprichii and A. nobilis) in Kavaratti atoll from February to March 2018. These species were observed in situ for oocyte maturation, and the larvae of species A. muricata and A. cytherea were assessed for survival and settlement rates. Observations on oocyte maturation indicated possible spawning closer to the immediate full moon of species in which 7–28% of the colonies had mature oocytes. Thus, A. muricata, A. cytherea and A. hemprichii spawned on 25 and 26 February 2018, demonstrating multi-specific synchronous spawning, whereas A. nobilis spawned on 21 March 2018. Larval survival rates revealed a steep die-off beginning on day 12 posts-pawning and maximum survival up to 24–27 days. Settlement occurred between 12 and 20 days for A. muricata and between 12 and 22 days for A. cytherea. The comparatively low survival duration and fewer larvae surviving for settlement show that maximum settlement could be heavily compromised. However, the study reveals that the comparatively late onset of settlement (from day-12, post-spawning) and the broader settlement window of 8–10 days could allow room for long-distance dispersal of larvae. Further studies on this front are required to gather a better picture.

The compound eyes of ancestral flies picked up only one picture point in each facet. The evolution of a means to split up the light-sensitive cells increased this number to seven, boosting the eye's resolution greatly. [PUBLICATION ABSTRACT]

The burden of type 2 diabetes (T2DM) in East Asia is alarming. Rapid modernization and urbanization have led to major lifestyle changes and a tremendous increase in the prevalence of obesity, metabolic syndrome, and diabetes mellitus. The development of T2DM at a younger age, with lower body mass index, higher visceral adiposity, and more significant pancreatic beta-cell dysfunction compared to Caucasians are factors responsible for the increased prevalence of T2DM in East Asians. Sodium-glucose Cotransporter-2 (SGLT2) inhibitors (canagliflozin, dapaglifozin, empagliflozin, etc.) reduce renal glucose reabsorption, leading to favorable effects on glycemic, blood pressure, and weight control. The insulin-independent mechanism enables their use as monotherapy or combination therapy with insulin and other oral antidiabetic agents. The role of SGLT2 inhibitors in the management of T2DM among East Asians is an interesting area of research, given that East Asians have been proven to be uniquely different from Caucasians. This review provides comprehensive coverage of the available literature not only on the efficacy and safety, but also on the recent cardiovascular and renal outcomes of SGLT2 inhibitors, focusing among East Asians.

Berry syndrome is an extremely rare constellation of several congenital cardiac anomalies consisting of aortopulmonary window, aortic origin of the right pulmonary artery (AORPA), interrupted aortic arch or hypoplastic aortic arch or coarctation of the aorta, and an intact ventricular septum with high neonatal mortality rates. The disease is fatal with high mortality (90) in the neonatal period with surviving patients mostly developing pulmonary hypertension. We describe the clinical presentation and diagnostic clues in two patients with Berry syndrome.

The compound eyes of ancestral flies picked up only one picture point in each facet. The evolution of a means to split up the light-sensitive cells increased this number to seven, boosting the eye's resolution greatly. An eye for an eye It's not often that you can glimpse the 'blind watchmaker' at work, says Kevin Moses in News and Views. The work he's referring to is the transition from the compound eyes found in ancestral flies and in some modern-day insects such as bees and beetles, where the light-sensing cells or rhabdomeres are fused together and function as a unit, to the type found in fruitfly and housefly eyes, where rhabdomeres act independently so that each facet of the lens perceives seven points of light instead of one. Zelhof et al . have identified three genes involved in rhabdomere assembly. The loss of one gene, called spacemaker , converts Drosophila 's open system to a closed or fused-rhabdomere system.

In the developing Drosophila eye, the morphogenetic furrow is a developmental organizing center for patterning and cell proliferation. The furrow acts both to limit eye size and to coordinate the number of cells to the number of facets. Here we report the molecular and functional characterization of Drosophila mini-me (mnm), a potential regulator of cell proliferation and survival in the developing eye. We first identified mnm as a dominant modifier of hedgehog loss-of-function in the developing eye. We report that mnm encodes a conserved protein with zinc knuckle and RING finger domains. We show that mnm is dispensable for patterning of the eye disc, but required in the eye for normal cell proliferation and survival. We also show that mnm null mutant cells exhibit altered cell cycle profiles and contain excess nucleic acid. Moreover, mnm overexpression can induce cells to proliferate and incorporate BrdU. Thus, our data implicate mnm as a regulator of mitotic progression during the proliferative phase of eye development, possibly through the control of nucleic acid metabolism.