Anomalous Transport Properties in BiS2-based Superconductors LnO1−xFxBiS2 (Ln = Nd, La-Sm)

We report the electronic properties of the layered bismuth-based sulfide superconductors NdO1−xFxBiS2 (x = 0.25, 0.4, and 0.5) and La1−ySmyO0.5F0.5BiS2 (y = 0.1–0.7), which have been studied by investigation of their transport properties and X-ray diffraction. In the lightly carrier-doped NdO1−xFxBiS2 (x = 0.25 and 0.4) and La1−ySmyO0.5F0.5BiS2 (y = 0.3 and 0.4), the resistivity and Hall coefficient exhibit anomalous temperature dependences below TCDW ∼ 130 and 200 K, respectively, suggesting the formation of an energy gap on the Fermi surface associated with charge-density wave (CDW). In NdO1−xFxBiS2 (x = 0.25), the bond angles and bond lengths of the Bi–S pentahedron change their temperature dependences below ∼200 K, suggesting that a lattice instability related to the Bi–S pentahedron exists below ∼200 K, which is much higher than TCDW. These results indicate that the lattice instability of the Bi–S pentahedron can trigger a CDW transition in the low-carrier region of BiS2 superconductors

Flt1/VEGFR1 heterozygosity causes transient embryonic edema

Vascular endothelial growth factor-A is a major player in vascular development and a potent vascular permeability factor under physiological and pathological conditions by binding to a decoy receptor Flt1 and its primary receptor Flk1. In this study, we show that Flt1 heterozygous (Flt1+/−) mouse embryos grow up to adult without life-threatening abnormalities but exhibit a transient embryonic edema around the nuchal and back regions, which is reminiscent of increased nuchal translucency in human fetuses. Vascular permeability is enhanced and an intricate infolding of the plasma membrane and huge vesicle-like structures are seen in Flt1+/− capillary endothelial cells. Flk1 tyrosine phosphorylation is elevated in Flt1+/− embryos, but Flk1 heterozygosity does not suppress embryonic edema caused by Flt1 heterozygosity. When Flt1 mutants are crossed with Aspp1−/− mice which exhibit a transient embryonic edema with delayed formation and dysfunction of lymphatic vessels, only 5.7% of Flt1+/−; Aspp1−/− mice survive, compared to expected ratio (25%). Our results demonstrate that Flt1 heterozygosity causes a transient embryonic edema and can be a risk factor for embryonic lethality in combination with other mutations causing non-lethal vascular phenotype

A modified Larson’s method of posterolateral corner reconstruction of the knee reproducing the physiological tensioning pattern of the lateral collateral and popliteofibular ligaments

<p>Abstract</p> <p>Background</p> <p>Consensus has been lacking as to how to reconstruct the posterolateral corner (PLC) of the knee in patients with posterolateral instability. We describe a new reconstructive technique for PLC based on Larson's method, which reflects the physiological load-sharing pattern of the lateral collateral ligament (LCL) and popliteofibular ligament (PFL).</p> <p>Findings</p> <p>Semitendinosus graft is harvested, and one limb of the graft comprises PFL and the other comprises LCL. Femoral bone tunnels for the LCL and popliteus tendon are made at their anatomical insertions. Fibular bone tunnel is prepared from the anatomical insertion of the LCL to the proximal posteromedial portion of the fibular head, which corresponds to the insertion of the PFL. The graft end for popliteus tendon is delivered into the femoral bone tunnel and secured on the medial femoral condyle. The other end for LCL is passed through the fibular tunnel from posterior to anterior. While the knee is held in 90 of flexion, the graft is secured in the fibular tunnel using a 5 mm interference screw. Then, the LCL end is passed into the femoral bone tunnel and secured at the knee in extension.</p> <p>Conclusions</p> <p>Differential tension patterns between LCL and PFL is critical when securing these graft limbs. Intrafibular fixation of the graft using a small interference screw allows us to secure these two graft limbs independently with intended tension at the intended flexion angle of the knee.</p

Intracholecystic papillary neoplasm acquiring malignant characteristics and leading to multiple liver metastases: A case report

Abstract The mechanisms underlying the progression of intracholecystic papillary neoplasms (ICPNs) to gallbladder cancer and invasive cancer remain relatively unclear. In the present case, metastatic liver tumors were suspected in an 83‐year‐old man at presentation; however, the primary tumor was unknown. The patient died shortly thereafter as a result of rapid tumor progression. An autopsy revealed multiple liver, lung, and lymph node metastases. Additionally, a fragile papillary tumor with a high‐grade dysplastic epithelium with tubulopapillary morphology and admixed foci of a low‐grade dysplastic epithelium were detected at the fundus of the gallbladder. The well‐differentiated tubular adenocarcinoma had extensively invaded the wall's granular mucosal surface along with the solitary papillary tumor. Based on pathological findings, a diagnosis of an ICPN with an associated invasive carcinoma was established. This case is novel because it showed that an ICPN can progress aggressively