Stretch-Induced Spin-Cast Membranes Based on Semi-Crystalline Polymers for Efficient Microfiltration.

Microfiltration membranes derived from semi-crystalline polymers face various challenges when synthesized through the extrusion-casting technique, including the use of large quantities of polymer, long casting times, and the generation of substantial waste. This study focuses on synthesizing these membranes using spin-casting, followed by stretch-induced pore formation. Recycled high-density polyethylene (HDPE) and virgin polyethylene powder, combined with a calcium carbonate filler, were used as the source materials for the membranes. The influence of the polymer-filler ratio with and without stretching on the morphology, tensile strength, and water flow rate was investigated. Optimal conditions were determined, emphasizing a balance between pore structure and mechanical integrity. The permeable membrane exhibited a water flow rate of 19 mL/min, a tensile strength of 32 MPa, and a water contact angle of 126°. These membranes effectively eliminated suspended particles from water, with their performance evaluated against that of commercially available membranes. This research, carried out utilizing the spin-casting technique, outlines a synthesis route for microfiltration membranes tailored to semi-crystalline polymers and their plastic forms.

Adsorbent-Embedded Polymeric Membranes for Efficient Dye-Water Treatment.

Traditional bulk adsorbents, employed for the removal of dyes and metal ions, often face the drawback of requiring an additional filtration system to separate the filtrate from the adsorbent. In this study, we address this limitation by embedding the adsorbent into the polymer matrix through a process involving dissolution-dispersion, spin-casting, and heat-stretching. Selective dissolution and dispersion facilitate the integration of the adsorbent into the polymer matrix. Meanwhile, spin-casting ensures the formation of a uniform and thin film structure, whereas heat-induced stretching produces a porous matrix with a reduced water contact angle. The adsorbent selectively captures dye molecules, while the porous structure contributes to water permeability. We utilized inexpensive and readily available materials, such as waste polyethylene and calcium carbonate, to fabricate membranes for the removal of methylene blue dye. The effects of various parameters, such as polymer-adsorbent ratio, initial dye concentration, and annealing temperature, were investigated. Equilibrium data were fitted to Langmuir, Freundlich, Temkin, and Dubinin-Radushkevich isotherms. The equilibrium data were best represented by the Langmuir isotherm, with maximum adsorption capacity of 35 mg/g and 43 mg/g at 25 °C and 45 °C, respectively. The membranes can be regenerated and recycled with a 97% dye removal efficiency. The study aims to present a template for adsorbent-embedded polymeric membranes for dye removal, in which adsorbent can be tailored to enhance adsorption capacity and efficiency.

Testosterone therapy, thrombophilia, and hospitalization for deep venous thrombosis-pulmonary embolus, an exploratory, hypothesis-generating study.

Our hypothesis was that testosterone therapy (TT) interacts with previously undiagnosed thrombophilia-hypofibrinolysis, leading to hospitalization for deep venous thrombosis (DVT)-pulmonary emboli (PE). We determined the prevalence of DVT-PE associated with TT 147 men hospitalized in the last 12 months for DVT-PE. Of the 147 men, 2 (1.4%) had TT before and at the time of their DVT-PE. Neither had risk factors for thrombosis. Neither smoked. Case #1 (intramuscular T 50mg/week) had 2 PE, 6 and 24 months after starting TT. DVT-PE in case #2 (T gel 100mg/day) occurred 24 months after starting T. Both men were found to have previously undiagnosed familial thrombophilia (protein S deficiency, homocysteinemia, high Factor VIII). In case #2, on 100mg T gel/day, serum estradiol was high, 51 pg/ml (upper normal limit 42.6 pg/ml). At least 1.4% of men hospitalized for DVT-PE were on TT and had previously undiagnosed thrombophilia, suggesting a thrombotic interaction between exogenous T and thrombophilia-hypofibrinolysis. Given the increasing use of TT, our preliminary findings should facilitate design of a much-needed, multi-center, prospective study of pro-thrombotic interactions between T therapy and thrombophilia for subsequent thrombotic events including DVT-PE.

Testosterone, thrombophilia, thrombosis.

We assessed previously undiagnosed thrombophilia-hypofibrinolysis in 11 testosterone (T)-taking men, five of whom developed deep venous thrombosis (DVT), four pulmonary embolism, one spinal cord infarction, and one osteonecrosis 3.5 months (median) after starting T gel (50-160 mg/day) or T intramuscular (50-250 mg/week). In the order of referral because of thrombosis after starting T, thrombophilia-hypofibrinolysis was studied in 11 men, and, separately, in two control groups without thrombosis - 44 healthy normal male controls and 39 healthy men taking T. Nine men had DVT or DVT-pulmonary embolism after 3.5 months (median) on T, one spinal cord infarction after 5 days on T, and one had osteonecrosis (knee and then hip osteonecrosis after 6 and 18 months on T). Four of the 11 men (36%) had high factor VIII (≥150%) vs. one of 42 (2%) controls (P = 0.005), and vs. one of 25 (4%) T-controls, (P = 0.023). Of the 11 men, two (18%) had factor V Leiden heterozygosity vs. none of 44 controls, (P = 0.04) and vs. none of 39 T-controls(P = 0.045). Of the 11 men, three had 4G4G plasminogen activator inhibitor-1 homozygosity, one prothrombin G20210A heterozygosity, one low protein S, and one high factor XI. When T was continued, second DVT-pulmonary embolism recurred in three of 11 men despite adequate anticoagulation. T interacts with thrombophilia-hypofibrinolysis leading to thrombosis. Men sustaining DVT-pulmonary embolism-osteonecrosis on T should be studied for thrombophilia. Continuation of T in thrombophilic men appears to be contraindicated because of recurrent thrombosis despite adequate anticoagulation. Before starting T, to prevent T-associated thrombosis, we recommend measures of factor V Leiden, factor VIII, and the prothrombin gene.