Object The pathogenesis of intraneural ganglia has been a controversial issue for longer than a century. Recently the authors identified a stereotypical pattern of occurrence of peroneal and tibial intraneural ganglia, and based on an understanding of their pathogenesis provided a unifying articular explanation. Atypical features, which occasionally are observed, have offered an opportunity to verify further and expand on the authors' proposed theory. Methods Three unusual cases are presented to exemplify the dynamic features of peroneal and tibial intraneural ganglia formation. Results Two patients with a predominant deep peroneal nerve deficit shared essential anatomical findings common to peroneal intraneural ganglia: namely, 1) joint connections to the anterior portion of the superior tibiofibular joint, and 2) dissection of the cyst along the articular branch of the peroneal nerve and proximally. Magnetic resonance (MR) images obtained in these patients demonstrated some unusual findings, including the presence of a cyst within the tibial and sural nerves in the popliteal fossa region, and spontaneous regression of the cysts, which was observed on serial images obtained weeks apart. The authors identified a clinical outlier, a case that could not be understood within the context of their previously reported theory of intraneural ganglion cyst formation. Described 32 years ago, this patient had a tibial neuropathy and was found at surgery to have tibial, peroneal, and sciatic intraneural cysts without a joint connection. The authors' hypothesis about this case, based on their unified theory, was twofold: 1) the lesion was a primary tibial intraneural ganglion with proximal extension followed by sciatic cross-over and distal descent; and 2) a joint connection to the posterior aspect of the superior tibiofibular joint with a remnant cyst within the articular branch would be present, a finding that would help explain the formation of different cysts by a single mechanism. The authors proved their hypothesis by careful inspection of a recently obtained postoperative MR image. Conclusions These three cases together with data obtained from a retrospective review of the authors' clinical material and findings reported in the literature provide firm evidence for mechanisms underlying intraneural ganglia formation. Thus, expansion of the authors' unified articular theory permits understanding and elucidation of unusual presentations of intraneural cysts. Whereas an articular connection and fluid following the path of least resistance was pivotal, the authors now incorporate dynamic aspects of cyst formation due to pressure fluxes. These basic principles explain patterns of ascent, cross-over, and descent down terminal nerve branches based on articular connections, paths of diminished resistance to fluid flow within recognized anatomical compartments, and the effects of fluctuating pressure gradients.

This study aimed to purify and identify antioxidant peptides from the low-molecular-weight fraction (SPH-I, MW < 3 kDa) of Alcalase-hydrolyzed soybean (Glycine max L.) hydrolysate and further evaluate the cytoprotective effects of synthesized peptides against oxidative stress in human intestinal Caco-2 cells. After purification by gel filtration chromatography and reversed-phase HPLC, four major peptides were sequenced by nano-LC-ESI-MS/MS as VVFVDRL (847 Da, SPH-IA), VIYVVDLR (976 Da, SPH-IB), IYVVDLR (877 Da, SPH-IC), and IYVFVR (795 Da, SPH-ID). The antioxidant peptides were synthesized and displayed desirable DPPH radical-scavenging activity (from 16.5 ± 0.5 to 20.3 ± 1.0 μM Trolox equivalent (TE)/μM), ABTS •+ radical-scavenging activity (from 3.42 ± 0.2 to 4.24 ± 0.4 mM TE/μM), ORAC (from 143 ± 2.1 to 171 ± 4.8 μM TE/μM), and FRAP (from 54.7 ± 1.2 to 79.0 ± 0.6 mM Fe 2+ /μM). Moreover, the synthesized peptides protected Caco-2 cells against H 2 O 2 -induced oxidative damage via significantly downregulating intracellular ROS generation and lipid peroxidation (p < 0.05). Additionally, SPH-IC and SPH-ID statistically upregulated total reduced glutathione synthesis, enhanced activities of catalase and glutathione reductase, and suppressed ROS-mediated inflammatory responses via inhibiting interleukin-8 secretion (p < 0.05).

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Six heat shock protein (HSP) genes from five HSP families in the parasitoid, Pteromalus puparum, were evaluated for their response to temperature (-15 ~ 3°C , and 30 ~ 42°C for 1 h), heavy metals (0.5 ~ 5 mM Cd(2+) and Cu(2+) for 24 h and 60 h), and starvation (24 h). Compared with other insect HSPs, all conserved motifs are found in P. puparum HSPs, and they are very similar to those of the recently sequenced ectoparasitoid Nasonia vitripennis. The temporal gene expression patterns indicated that these six HSP genes were all heat-inducible, of which hsp40 was the most inducible. The temperatures for maximal HSP induction at high and low temperature zone were 36 or 39°C and -3°C, respectively. In the hot zone, all HSP genes have the same initial temperature (33°C) for up-regulation. Low concentrations of Cd(2+) for a short-term promoted the expression of all HSP genes, but not high concentrations or long-term treatments. Cu(2+) stress for 24 h increased expression of nearly all HSP. Four HSP genes changed after starvation. We infer that all six HSP genes are sensitive to heat. This may help understand the absence of P. puparum during the summer and winter. The expression profiles of six HSP genes in P. puparum under heavy metal stress indicates that HSP is a short-term response to cellular distress or injury induced by Cd(2+) and Cu(2+).