Reconstruction of both eyelids following electrical burn

A case of severe electrical burn of the unilateral upper and lower eyelids is reported, together with the surgical technique of reconstruction. A 25-year-old man suffered an electrical burn on his left eyelids. On admission, his left upper and lower eyelids were subtotally necrotic. Total eyelid reconstruction was performed 2 1/2 months later. A chondromucosal graft taken from the nasal septum was utilized as the deep layer of the upper eyelid, which was covered by sliding down the remaining levator muscle and connective tissues to maintain the blood supply to the composite graft. The outer layer of the upper lid was reconstructed with a free split-thickness skin graft. The lower lid was reconstructed with a local flap lined with a free mucosal graft. This sandwich method using the levator muscle as a core was found useful for reconstructing both the upper and lower eyelids.     

广东省国家I级重点保护野生植物资源现状及保护策略

在查找史料的基础上,根据国家重点保护植物名录(第一批),确定了在广东有分布的仙湖苏铁、银杏、南方红豆杉、合柱金莲木、伯乐树、报春苣苔、水松、异形玉叶金花和台湾苏铁9种国家I级重点保护植物作为调查对象,在全省开展了较为全面的调查。结果只找到了前6种,植株数量合计为123468株。除仙湖苏铁和报春苣苔分布地点没有变化外,其他7种的分布地点丧失率在20%-100%之间。除南方红豆杉基本上属于正常种群外,其余8种分属于野外绝迹、濒临绝迹或濒危类物种,其资源状况堪忧。在对其资源现状进行详细分析的基础上,提出了相应的保护管理策略和发展措施。     

Myosin light chain kinase mediates intestinal barrier disruption following burn injury

Background

Severe burn injury results in the loss of intestinal barrier function, however, the underlying mechanism remains unclear. Myosin light chain (MLC) phosphorylation mediated by MLC kinase (MLCK) is critical to the pathophysiological regulation of intestinal barrier function. We hypothesized that the MLCK-dependent MLC phosphorylation mediates the regulation of intestinal barrier function following burn injury, and that MLCK inhibition attenuates the burn-induced intestinal barrier disfunction.

Methodology/Principal Findings

Male balb/c mice were assigned randomly to either sham burn (control) or 30% total body surface area (TBSA) full thickness burn without or with intraperitoneal injection of ML-9 (2 mg/kg), an MLCK inhibitor. In vivo intestinal permeability to fluorescein isothiocyanate (FITC)-dextran was measured. Intestinal mucosa injury was assessed histologically. Tight junction proteins ZO-1, occludin and claudin-1 was analyzed by immunofluorescent assay. Expression of MLCK and phosphorylated MLC in ileal mucosa was assessed by Western blot. Intestinal permeability was increased significantly after burn injury, which was accompanied by mucosa injury, tight junction protein alterations, and increase of both MLCK and MLC phosphorylation. Treatment with ML-9 attenuated the burn-caused increase of intestinal permeability, mucosa injury, tight junction protein alterations, and decreased MLC phosphorylation, but not MLCK expression.

Conclusions/Significance

The MLCK-dependent MLC phosphorylation mediates intestinal epithelial barrier dysfunction after severe burn injury. It is suggested that MLCK-dependent MLC phosphorylation may be a critical target for the therapeutic treatment of intestinal epithelial barrier disruption after severe burn injury.     

Activation/inactivation of human angiotensin I converting enzyme following chemical modifications of amino groups near the active site

We have studied the effects of amidination of lysyl residues on the activity of angiotensin I converting enzyme isolated from human kidney. Anion concentration was an important reaction variable. In 4 M chloride or acetate, amidination with methyl acetimidate produced derivatives with up to a 4-fold increase in activity with hippuryl-glycyl-glycine as substrate. Modification with methyl p-hydroxybenzimidate also increased activity while treatment with methyl 4-mercaptobutyrimidate resulted in a 90% loss of activity. The effects of amidination were partially prevented when the reactions were carried out in the presence of the inhibitors, captopril or 5S-benzamido-4-oxo-6-phenyl-hexanoyl-L-proline. These results suggest that lysyl residues are present near the active site while different amino groups have a role in anion activation.     

Trace elements in chemical evolution,I

Research on trace elements in chemical evolution is reviewed from three points of view. They are:(i) the origin of the essentiality of trace elements in present biological systems; (ii) the possible roles of trace elements in chemical evolution; and (iii) the origin of enzymatic activity with metal ions,i.e., the origin of metalloenzymes.     

Stability of fibronectin biological activity following chemical modification

Fibronectin isolated from human plasma functions in vitro as a mediator of adhesion and spreading of trypsinized fibroblasts on native or denatured collagen. As a means of elucidating structural characteristics which might contribute to fibronectin's biological activity, we have modified and digested the protein with several chemicals. Following various treatments, the protein was utilized to mediate cell adhesion and spreading on collagen to determine which alteration disrupted its activity. Fibronectin remained functionally intact after partial or complete reduction and alkylation, oxidation of 59% of the carbohydrates with sodium periodate, citraconylation, carbodiimide-catalyzed amide formation, and oxidation of 35.2 residues of tryptophan/molecule with N-bromosuccinimide. Dinitrofluorobenzene treatment, which phenylated ten residues/molecule of fibronectin, successfully inactivated fibronectin's in vitro biological function. Effective modification of the protein was determined by appropriate analytical procedures. Since fibronectin retained its biological function after several treatments that presumably affected its molecular conformation, we concluded that its secondary or tertiary structure appears not to be essential for its in vitro activity, or alternatively that the protein possesses a biologically active domain relatively resistant to chemical modification.     

Ultrastructural changes in adrenergic neurons following chemical sympathectomy

The paper describes the ultrastructural changes of the sympathetic neurons following guanethidine administration in mice. The main characteristics changes, after prolonged administration (1-10 weeks) of guanethidine (Ismelin, Ciba-Geigy, Basel, Switzerland) at doses of 30-50 mg/kg/day i.p. and i.m. were: (1) Mitochondrial damages: swelling and deformation of the mitochondria, with disruption and dispersion of the cristae and condensation or dissolution of the matrix. Membranolysis of the outer and inner mitochondrial membranes. (2) Neural processes: swelling and disorganization of the internal architecture in the postganglionic axonal and dendritic synaptic varicosities. (3) Adrenergic vesicles: disappearance of the granular vesicles in the early stage of the experiment, increase of the coated vesicles in the later stage of treatment. The effect of guanethidine is specific for the postganglionic adrenergic neurons, but the observed destruction is not caused solely by guanethidine; other chemical substances induce the same or similar degeneration in the sympathetic ganglion.     

Mutation frequency decline following chemical mutagenesis of Salmonella typhimurium

The occurrence is reported of a mutation frequency decline process (MFD) following treatment of Salmonella typhimurium strain trpC₃ with two chemical mutagens which give rise predominantly to suppressor revertants. With the carcinogen 4-nitroquinoline-N-oxide (4NQO) the results are analogous to those obtained for UV-mutagenesis. In the case of methoxynamine, the process is due to specific excision of premutational lesions, since lethality is low and lethal lesions are non-excisable. Mutants are described which cannot perform MFD of lesions induced by one or both of the chemical mutagens, indicating that the loss of revertants is in each case due to a bacteial repair system rather than to spontaneous degradation of the induced lesion. The mutants, however, were isolated because of an altered response to UV mutagenesis, viz., their ability to express UV-induced mutants in the absence of amino acids to stimulate active post-irradiation protein synthesis. In all other respects tested, their response to UV is identical with that of the parent strain. The hypothesis is discussed that the total absence of UV-induced revertants of the strain S. typhimurium trpC₃ when active protein synthesis is inhibited is due to two processes, first, rapid MFD due to the specific excision of pyrimidine dimers (the predominant UV-lesion) and secondly, the slow excision of other premutational damage which may be other photoproducts or secondary distortions caused by close juxtaposition of several pyrimidine dimers.