A case of skin ulcers secondary to extensive burns caused by flame and heavy metal-containing hydrothermal fluids / 中华烧伤杂志

On May 13, 2020, a 56-year-old man with extensive burns caused by flames and heavy metal-containing hydrothermal fluids was admitted to the General Hospital of Western Theater Command. After being admitted to the hospital, most of the burn wounds healed after treatments such as debridement, expansion, skin grafting, anti-shock, anti-infection, fluid replacement, and wound dressing change, etc. However, in the middle and late stages of treatment, the patient's burn wounds gradually showed repeated skin ulceration and inflammation. After excluding the cause of physical, bacterial infection and others, IgG4-related skin diseases was finally diagnosed by histopathological examination of tissue biopsy and concentration measurement of IgG4 in interstitial fluid, and the condition was improved after hormone treatment. This suggests that extensive burns may lead to the occurrence of autoimmune skin diseases. For the diagnosis of such diseases, it is necessary to combine clinical manifestations, serological examinations, and histopathological biopsy, etc. to avoid diagnostic pitfalls and draw correct conclusions.

Effects of neuroactive steroid allopregnanolone on the damage of cortical neurons / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To investigate the protective mechanism of neuroactive steroid allopregnanolone on N-methyl-D-aspartate (NMDA) induced toxicity in primary mouse cortical neurons.</p><p><b>METHODS</b>Primary cultured mouse cortical neurons were subjected to allopregnanolone, the expression of beta-aminobutyric acid receptor beta2 subunit (beta2-GABA-R) mRNAs was detected by RT-PCR and Akt phosphorylation was assayed by Western blot using Akt-phosphoserine 473-specific antibody. After the cultured mouse cortical neurons were pretreated with or without allopregnanolone prior to treatment with NMDA , DNA isolated was analyzed by agarose gel electrophoresis and proteins collected were analyzed by Western blot with anti-cleaved-PARP, anti-cleaved caspase-3, and anti-cleaved caspase-9 antibodies.</p><p><b>RESULTS</b>When cultured mouse cortical neurons were exposed to allopregnanolone both the expression of beta2-GABA-R mRNAs and Akt phosphorylation increased. Allopregnanolone inhibited the NMDA-induced apoptosis and decreased the level of active-PARP, active-caspase-3 and active-caspase-9 notably at a final concentration of 5 x 10(6) mol/L.</p><p><b>CONCLUSION</b>Pretreatment with allopregnanolone may be neuroprotective on NMDA-induced neuronal cells apoptosis by increasing beta2-GABA-R expression and Akt phosphorylation.</p>

Influence on costal cartilage reparative regeneration by replanting the small blocks of autogeneic cartilage / 中华整形外科杂志

<p><b>OBJECTIVE</b>To investigate the influence on costal cartilage reparative regeneration by replanting the small blocks of autogeneic cartilage into the perichondrial pocket at the donor-site.</p><p><b>METHODS</b>16 rabbits (8-10 weeks old, 1.8-2.2 kg) were randomly divided into four groups as three experimental groups and one control group. The 1.5 cm in length of costal cartilage defect was made in experimental groups with the perichondrium and costochondral junction left completely intact. The cartilage defect was closed by 3 methods as saturation directly, or replanting the small blocks of autogeneic cartilage, or plugging bio-protein jelly after cartilage replanting. Each experimental group was handled with two methods in two sides of costal cartilage. No operation was performed in control group. All the rabbits were sacrificed 16 weeks after operation. The appearance of thoracic cage and new-formed tissue at the defect site were examined grossly. Haematoxylin-eosin staining was performed to evaluate the characteristics of new-formed tissues and biomechanical detection was used to measure intension of new-formed tissues.</p><p><b>RESULTS</b>The appearance of thoracic cage was normal in every experimental group. Histological study showed that the defect was filled with abundant fibrous tissue in each group. The chipping of cartilage survived effectively with little proliferation. Biomechanical detection showed that the intension of new-formed tissue in the non-replanted group [(193.92 +/- 41.41) N] was obviously less than that in the replanted group [(318.88 +/- 28.28) N], or bio-protein jelly group [(301.00 +/- 39.52) N], or control group [(300.54 +/- 38.35) N] (P < 0.01). Furthermore, there was no statistical difference between the latter three groups (P > 0.05).</p><p><b>CONCLUSIONS</b>Although replanting the chipping of cartilage can't promote reparative regeneration of hyaline cartilage, it can definitively strengthen the intensity of new-formed tissue, reinforce thoracic stability. It may also indirectly decrease the incidence rate of postoperative chest wall deformity.</p>

Allicin can reduce neuronal death and ameliorate the spatial memory impairment in Alzheimers disease models

To investigate the mechanisms and protective effects of allicin on learning and memory in a mouse model of Alzheimer's disease [AD]. This study took place in the Institute of Medicine of Jishou University, Jishou, China, between January and September 2009. Allicin was given as preventive administration after AD was induced by amyloid beta [A beta [1-42]], and the protective effects of Allicin against learning and memory impairment were investigated. Sixty mice were randomly divided into 3 groups including the sham-operated+phosphate buffer solution [PBS] group, the A beta [1-42]+PBS group, and the A beta [1-42]+allicin group. The A beta [1-42] [1 micro L = 4 micro g] was injected into the bilateral hippocampi. Sham-operated mice were infused with PBS. Allicin or PBS was then injected intraperitoneally for 14 days. The animals were trained, and learning and memory abilities tested using the Morris Water-Maze. The changes of A beta [1-42] and P38 mitogen-activated protein kinase [p38MAPK] were recorded to explore the mechanism of allicin's protective effects on learning and memory deficits. The A beta [1-42]-infused allicin-treated group showed significantly shorter latency times than the PBS treated A beta [1-42]-infused group from the second day of learning sessions [p=0.031], accompanied with significant reduction of malondialdehyde [MDA] [p=0.035] and an increase of superoxide dismutase [SOD] activity [p=0.041]. Allicin also decreased A beta and p38MAPK expressions in the cerebral cortex of AD mice model [p=0.031]. Preventive administration of allicin prevented learning and memory impairment, the mechanism may be due to an increase in the activity of SOD, a reduction in the levels of MDA and the expressions of A beta and p38MAPK in the brain