Function of human serum albumin and its application in therapy of critical illness / 解放军医学杂志

Human serum albumin (HSA) is a small molecule, non-glycosylated, negatively charged serum protein, and due to its flexible structure it possesses multiple functions, such as it acts as a carrier in the plasma by binding and transporting various substances, helps preserve the integrity of vascular endothelium, and it also possesses functions of anti-oxidation, anti-inflammation, protection of organ function, and maintenance of colloid osmotic pressure. HSA has been used as a therapeutic agent for critical ill patients for a long time. Comprehensive and meta analysis based on previous studies revealed that HSA has a certain effect in lowering incidence of complications in the treatment of critical disease. For some diseases, like sepsis, hepatocirrhosis complicated with spontaneous bacterial peritonitis, etc., the use of HSA can significantly improve the prognosis of the patient, however, its positive role in reducing overall mortality rate is still undetermined.

Function of human serum albumin and its application in therapy of critical illness / 解放军医学杂志

Human serum albumin (HSA) is a small molecule, non-glycosylated, negatively charged serum protein, and due to its flexible structure it possesses multiple functions, such as it acts as a carrier in the plasma by binding and transporting various substances, helps preserve the integrity of vascular endothelium, and it also possesses functions of anti-oxidation, anti-inflammation, protection of organ function, and maintenance of colloid osmotic pressure. HSA has been used as a therapeutic agent for critical ill patients for a long time. Comprehensive and meta analysis based on previous studies revealed that HSA has a certain effect in lowering incidence of complications in the treatment of critical disease. For some diseases, like sepsis, hepatocirrhosis complicated with spontaneous bacterial peritonitis, etc., the use of HSA can significantly improve the prognosis of the patient, however, its positive role in reducing overall mortality rate is still undetermined.

Effect of intensive insulin therapy on apoptosis-related ligands in serum in rats with severe scald / 中华烧伤杂志

<p><b>OBJECTIVE</b>To investigate changes in apoptosis-related ligands in serum in rats with severe scald and the effect of intensive insulin therapy on the changes.</p><p><b>METHODS</b>One hundred and fifty Wistar rats were randomly divided into 3 groups: sham burn (SB), scald (S) and treatment (T) groups. Rats in S and T groups were inflicted with 40% TBSA full-thickness burn, followed by intraperitoneal injection with 40 mL/kg of isotonic saline for resuscitation. Rats in T group were subcutaneously injected insulin in a dose of 0.25 U/100 g 24 hours after burn injury, and every 12 hours for 5 days (0.25, 0.50, 0.75, 1.00, 1.25 U/100 g each day, respectively) to control the level of blood glucose between 3 and 6 mmol/L. Rats in SB group were sham scalded at 37 degrees C without resuscitation. Blood was drawn from abdominal aorta on 1, 4, 7, 10, 14 post burn day (PBD) for determination of serum levels of TNF-alpha, soluble Fas ligand (sFasL) and soluble Fas receptor (sFas) by enzyme-linked immunosorbent assay (ELISA), and insulin by radioimmunity assay (RIA).</p><p><b>RESULTS</b>The serum level of TNF-alpha in S group peaked on 1 PBD (30.9 +/- 8.7) ng/L, which showed statistically significant difference when compared with that of SB and T groups (12.7 +/- 2.8) ng/L, (16.8 +/- 4.7) ng/L, respectively, P < 0.01), then lowered gradually to become similar to that of SB group on 7 PBD. The level of TNF-alpha in T group increased gradually, but was obviously lower than that of S group on 1, 4, 7 PBD (P < 0.01). The level of sFasL in S (on 7-14 PBD) and T (4-10 PBD) groups was significantly higher than that in SB group (P < 0.05), then lowered to normal level. The levels of sFas on 4-10 PBD in T group were obviously higher than that in S and SB group (P < 0.05). Ratio of sFasL to sFas in serum of S group was higher than that in SB group on 7, 10 PBD, which was higher than that in T group on 7 PBD (P < 0.05). There was significant decrease in serum level of insulin in S group compared with that of SB group on 4-10 PBD (P < 0.05). The level of insulin in T group increased on 1 PBD, peaked on 4 PBD (327 +/- 15 microU/mL), which was significantly higher than that in SB and S groups (42 +/- 15, 28 +/- 10 microU/mL, respectively, P < 0.01), then decreased gradually to normal level.</p><p><b>CONCLUSIONS</b>Insulin may inhibit apoptosis after burn by down-regulating secretion of apoptotic ligands.</p>

Changes in proliferative activity of myoblasts and expression of Akt in skeletal muscle of rats after severe burn injury / 中华外科杂志

<p><b>OBJECTIVE</b>To investigate changes in proliferative activity of myoblasts in skeletal muscle and potential role of phosphorylated Akt on it, so that a better understanding in mechanisms of skeletal muscle atrophy after burn injury will be got.</p><p><b>METHODS</b>One hundred and twenty Wistar rats were randomly divided into 2 groups: control and severe thermal injury group. Rats in severe thermal injury group were subjected to a 40% total body surface area full-thickness scald injury, and Tibialis Anterior (TA) muscles were collected on 0, 1, 4, 7, 10, 14 days post-injury. After muscle mass determined, immunohistochemical double staining was used for detection of Proliferative Cell Nuclear Antigen (PCNA) of myoblasts. Protein expression of total Akt and phosphorylated Akt was determined by Western Blot.</p><p><b>RESULTS</b>Burn injury induced significant reduction of TA muscle mass and maximal reduction of it appeared by 4 days after injury (P < 0.01). Proliferative activity of myoblasts decreased significantly from the first day post-injury (P < 0.01) and increased slowly to basal level of controls after 7 days post-injury. The phosphorylated Akt was undetectable in both of controls and injured samples before 4 days but increased significantly after 7 days post-injury (P < 0.01), though total Akt expression had no significant alteration at any time points (P > 0.05).</p><p><b>CONCLUSIONS</b>Decrease in proliferative activity of myoblasts may be one of the contributors of significant atrophy of skeletal muscle after burn injury. Effect of phosphorylated Akt on proliferation attenuated in early stage and increased significantly in later stage after burn injury may partly explain the changes in proliferative activity of myoblasts.</p>

Study on the injurious effect of a self designed micro-skin machine on the epithelia / 中华烧伤杂志

<p><b>OBJECTIVE</b>To observe the injury on micro-skin induced by a self designed micro-skin machine.</p><p><b>METHODS</b>Micro-skin was produced either with the machine or by hand. Cells at the edge of micro-skin were observed by transmission electron microscope. succinic dehydrogenase activity in supernatant of cultivated cells was analyzed, and the cell proliferation of micro-skin was assessed by (3)H-TdR. Twenty patients were enrolled in the study for the observation of the wound healing time between the two groups of micro-skin after being grafted.</p><p><b>RESULTS</b>Transmission electron microscope examination revealed that the cellular injury at the edge of the micro-skin in machine-made group was mild compared with that in man-made group. (3)H-TdR rate was elevated but the activity of succinic dehydrogenase in the supernatant of cultured cells decreased in supernatant of cultured cells of machine produced micro-skin. Wound healing time was shortened in machine made group. (P < 0.05).</p><p><b>CONCLUSION</b>The cellular injury at the edge of micro-skin in the machine made group was mild when compared with that in the man-made group with cell proliferation accelerated and wound healing time shortened.</p>

Investigation of p53 gene mutations in keloids using PCR-SSCP / 中华整形外科杂志

<p><b>OBJECTIVE</b>To detect gene mutations of p53 gene (exon 4-6) in fibroblasts.</p><p><b>METHODS</b>Samples of keloids were taken from 15 patients. The mutations of p53 gene were detected using polymerase chain reaction, the single-strand conformational polymorphism(SSCP) analysis and DNA sequencing.</p><p><b>RESULTS</b>Gene mutations in p53 gene exon 4, 5, and 6 were identified in all the patients with keloids.</p><p><b>CONCLUSION</b>Gene mutations resulted in keloid p53 protein losing its functions of suppressing cell processes and conducting apoptosis.</p>

Cell cycle analysis and P53 gene mutation detection of fibroblasts derived from the surrounding skin of keloids / 中华整形外科杂志

<p><b>OBJECTIVE</b>To investigate whether there are abnormal fibroblasts in the surrounding skin of keloids for better understanding of the etiological feature of keloids.</p><p><b>METHODS</b>Fresh samples were used for cell culture. Flow cytometry was used for analyzing cell cycles of fibroblasts derived from keloids and the surrounding skin. Proliferative cell proportions were compared between every two groups. P53 exon 4, 5 and 6 were amplified by PCR. DNA was sequenced to examine the structure of the destination gene.</p><p><b>RESULTS</b>The proliferative cell proportion of the fibroblasts derived from the surrounding skin is not so high as that from the verge of keloids, but is higher than the normal skin fibroblasts derived from other part of the keloid patients or persons without keloids (P < 0.05). Mutations (point and frameshift mutations) of P53 exon 4 (6/6) and exon 5(2/6) in fibroblasts derived from the surrounding skin of keloids were identified. Fibroblasts derived from keloids have the same mutations as its surrounding skin.</p><p><b>CONCLUSION</b>There are abnormal fibroblasts in the surrounding skin of keloids. It may be the consequence of keloid infiltrative growth and a reason of easy recurrence of keloid after therapy.</p>