Reconfigurable Metasurface: Enabling Tunable Reflection in 6G Wireless Communications.

With the continuous advancement of technology, there is an increasing need for innovative solutions that can handle complex applications such as haptic communications, Internet of Things for smart cities, automation, and manufacturing. One technology that has received much attention is the phase reconfigurable metasurface for reconfigurable intelligent surfaces (RISs). The RIS demands low-power consumption, simple configuration, angular stability, and polarization insensitivity. The use of phase reconfigurable metasurfaces provides benefits such as low cost, low power consumption, and improved communication coverage and quality. This article introduces a reconfigurable combined-loop metasurface that can effectively manipulate phase reflection. This is achieved by incorporating four PIN diodes between two meta-atoms of a 2 × 2 periodic array within a single-layer metallic structure. By controlling the state of the PIN diodes, which can be switched into 16 different states, the metasurface can achieve various phase reflections. The proposed structure has validated a 32× 32 metasurface through numerical simulations and experiments that exhibit promising results, demonstrating its potential for use in 6G applications.

Sensitivity and Robustness of Spatially Dependent Thrombin Generation and Fibrin Clot Propagation.

Blood coagulation is a delicately regulated space- and time-dependent process that leads to the formation of fibrin clots preventing blood loss upon vascular injury. The sensitivity of the coagulation network was previously investigated without accounting for transport processes. To investigate its sensitivity to coagulation factor deficiencies in a spatial reaction-diffusion system, we combined an in vitro experimental design with a computational systems biology model. Clot formation in platelet-free plasma supplemented with phospholipids was activated with identical amounts of tissue factor (TF) either homogeneously distributed (concentration 5 pM, homogeneous model) or immobilized on the surface (surface density 100 pmole/m2, spatially heterogeneous model). Fibrin clot growth and thrombin concentration dynamic in space were observed using video microscopy in plasma of healthy donors or patients with deficiencies in factors (F) II, FV, FVII, FVIII, FIX, FX, or FXI. In the spatially heterogeneous model, near-activator thrombin generation was decreased in FV-, FVII-, and FX-deficient plasma. In the homogeneous model, clotting was not registered in these samples. The simulation and experiment data showed that the coagulation threshold depended on the TF concentration. Our data indicate that the velocity of spatial clot propagation correlates linearly with the concentration of thrombin at the clot wave front but not with the overall thrombin wave amplitude. Spatial clot growth in normal plasma at early stages was neither reaction nor diffusion limited but became diffusion limited later. In contrast, clot growth was always diffusion limited in FV-, FVII-, and FX-deficient plasma and reaction limited in FVIII-, FIX-, and FXI-deficient plasma. We conclude that robustness of the spatially heterogeneous coagulation system was achieved because of the combination of 1) a local high TF surface density that overcomes activation thresholds, 2) diffusion control being shared between different active factors, and 3) an early saturated stimulus-response dependence of fibrin clot formation by thrombin.

Platelets provide robustness of spatial blood coagulation to the variation of initial conditions.

Activated platelets provide phospholipid surface and secrete coagulation factors, enhancing blood clotting. We investigated the role of platelets in the regulation of blood coagulation spatial dynamics. We activated blood clotting with tissue factor-bearing (TF) surface in platelet-rich plasma (PRP) or platelet-free plasma (PFP). When blood coagulation was initiated by high TF density, clot growth rate (V) in PRP (2 × 105/µL platelets) was only 15 % greater than in PFP. Spatial distribution of thrombin in PRP had a peak-like shape in the area of the fibrin clot edge, while in PFP thrombin was distributed in the shape of descending plateau. Platelet inhibition with prostaglandin E1 or cytochalasin D made spatial thrombin distribution look like in the case of PFP. Inhibition of blood coagulation by natural endogenous inhibitor heparin was diminished in PRP, while the effect of the exogenous or artificial inhibitors (rivaroxaban, nitrophorin, hirudin) remained undisturbed in the presence of platelets. Ten times decrease of the TF surface density greatly depressed blood coagulation in PFP. In PRP only clotting initiation phase was, while the propagation phase remained intact. Coagulation factor deficiency greatly reduced amount of thrombin and decreased V in PFP rather than in PPR. Thus, platelets were redundant for clotting in normal plasma under physiological conditions but provided robustness of the coagulation system to the changes in initial conditions.

Survival case of acute and severe respiratory distress due to spontaneous tension gastrothorax.

A 20-year-old woman presented with abdominal pain and shortness of breath. She was in obstructive shock with absent breath sounds on the left haemithorax. Chest X-ray showed a large radiolucent shadow with absent lung markings and mediastinal shift to the right side with concerns for tension pneumothorax. Though tube thoracostomy was done on the left side of the chest, column movement was absent. To confirm the diagnosis CT with contrast was done that revealed a huge left side diaphragmatic defect with abdominal contents in the thorax and mediastinal structures are shifted to left. She underwent emergency laparotomy and postoperative period was uneventful.