Use of lung ultrasound for the diagnosis and treatment of pleural effusion.

Pleural effusion affects gas exchange, hemodynamic stability, and respiratory movement, thereby increasing the failure rate of intensive care unit discharge and mortality. Therefore, it is especially important to diagnose pleural effusion quickly to make the appropriate treatment decisions. The present review discusses the role of ultrasound in the diagnosis and puncture/drainage of pleural effusions and highlights the importance of lung ultrasound techniques in this patient population. We searched on PubMed, Embase, and Cochrane Library databases for articles from establishment to October 2022 using the following keywords: "lung ultrasound", "pulmonary ultrasound", "pleural effusion", "ultrasound-guided" and "thoracentesis". Lung ultrasound not only helps clinicians visualize pleural effusion but also to identify its different types and assess pleural effusion volume. It is also very important for thoracentesis, not only to increase safety and reduce life-threatening complications, but also to monitor the amount of fluid after drainage of pleural effusion. Lung ultrasound is a simple, noninvasive bedside technique with good sensitivity and specificity for the diagnosis and treatment of pleural effusions.

Advances in the application of ultrasound for fracture diagnosis and treatment.

Fractures are commonly encountered in clinical practice. Early diagnosis and individualized treatment are the basis for achieving high-quality fracture healing and functional recovery. Radiographic examinations play an important role in the diagnosis and treatment of fractures. In recent years, with the innovation in ultrasonic examination technology and equipment, its application in the diagnosis and treatment of fractures has greatly increased. Long bone, rib, radius and ulnar, metacarpal, cartilage, nasal bone, and occult are common fracture types. Ultrasound has long been used in fracture diagnosis and treatment. This narrative review summarizes and discusses the application of ultrasound in the diagnosis and treatment of fractures.

Selection of peptide inhibitors for double-stranded RNA-dependent protein kinase PKR.

Protein kinase inhibitors have been developed and applied as antitumor drugs. The majority of these inhibitors are derived from ATP analogs with limited specificity towards the kinase target. Here we present our proof-of-principle study on peptide inhibitors for kinases. Two peptides were selected by phage display against double-stranded RNA-dependent protein kinase (PKR). In vitro assay revealed that these peptides exhibit an inhibitory effect on PKR-catalyzed phosphorylation of the alpha subunit of eukaryotic initiation factor 2 (eIF2α). The peptides also interrupt PKR activity in cells infected by viruses, as PKR activation is one of the hallmarks of host response to viral infection. Kinetic study revealed that one of the peptides, named P1, is a competitive inhibitor for PKR, while the other, named P2, exhibits a more complicated pattern of inhibition on PKR activity. Fragment-based docking of the PKR-peptide complex suggests that P1 occupies the substrate pocket of PKR and thus inhibits the binding between PKR and eIF2α, whereas P2 sits near the substrate pocket. The computational model of PKR-peptide complex agrees with their kinetic behavior. We surmise that peptide inhibitors for kinases have higher specificity than ATP analogs, and that they provide promising leads for the optimization of kinase inhibitors.

Effect of selenium on aflatoxin hepatocarcinogenesis in the rat.

The effects of selenium (Na2SeO3) on aflatoxin B1 (AFB1)-induced hepatic neoplasia were studied in the rat. Putative preneoplastic foci and nodules composed of basophilic, eosinophilic, and clear cells developed early. Basophilic foci were seen first; in the later stages basophilic and eosinophilic nodules predominated. At each stage the AFB1 + Se groups showed fewer and smaller foci and nodules than the AFB1 - Se group. The number of foci in the AFB1 + 3 ppm Se group and their mean area were smaller than those in the 6 ppm Se + AFB1 group. At the end of the experiment hepatocellular carcinoma (HCC) was found in 11/18 rats (61%) of the AFB1 - Se group. HCC was not found in either of the groups given AFB1 + Se. We conclude that Se had an inhibitory effect on the initiation and promotion stages of AFB1-induced preneoplastic foci and nodules. Se also prevented progression of these nodules to HCC even after cessation of AFB1 administration. The inhibitory effect of Se at 3 ppm was greater than at 6 ppm. The 6 ppm Se group also showed evidence of toxicity.

A study on the inhibition of aflatoxin B1 induced hepatocarcinogenesis by the Rhizopus delemar.

The effect of Rhizopus delemar on the carcinogenicity in rats of Aflatoxin B1 was studied. The Aflatoxin B1 was administered in free drinks to each male wistar rat at 126 micrograms per week such that a total dose of 3.40 mg was given over a period of 27 weeks. The culture abstract of Rhizopus delemar was added simultaneously to a group of these rats by mixing the Aflatoxin B1 solution. Animals were killed separately during 18th, 30th, 38th and 52nd week. Liver cell altered foci and neoplasms were qualified by using light microscopic and electromicroscopic morphology, by the morphometry and by the enzymic reactions. In the group of Aflatoxin B1 the incidence of hepatocellular carcinoma was 71%. In the group receiving Rhizopus delemar together with Aflatoxin B1, the hyperplastic foci and pathological enzymic foci were decreased at all times pointed and atd at termination, and in none of the rats had liver neoplasms appeared. The result of this experiment showed that the Rhizopus delemar has intensive capacity in inhibiting the toxic damage and carcinogenicity of the liver by the Aflatoxin B1, because it is not only able to postpone the appearance of altered foci and to control their development but also to accelerate their withdraw in advance. The Rhizopus delemar can be used as a feasible and efficacious means to control the intoxication of Aflatoxin B1.