Accumulation of Uridinediphospho-N-acetylmuramyl-peptides Induced by Glycine and Penicillin

The genes POX2 and POX4, which encode the subunits (PXP-2 and PXP-4) of peroxisomal fatty acyl-coenzyme A oxidase of Candida tropicalis, were introduced into the related yeast Candida maltosa. The cells transformed with POX2 or POX4 gave much PXP-2 or PXP-4 in the purified peroxisomes. The polypeptides associated with the heterologous organelle were resistant to added protease, implying that they were transported into the peroxisomes. Genes for curtailed versions of PXP-4 were constructed in vitro and introduced into the host cells. Peptide-C, the COOH-terminal two-thirds of PXP-4, was efficiently transported into the host peroxisomes, and the polypeptide containing the NH₂-terminal one-third was also, in much lesser amount. These and other results suggested that there were at least two regions of peroxisomal targeting information in PXP-4 and the primary information was internal. The deletions in Peptide-C inhibited the transport of many, but not all, of the host-cell peroxisomal polypeptides. This suggested heterogeneous transport systems on the peroxisomal membrane.     

Biophoton Emission Induced by Heat Shock

Ultraweak biophoton emission originates from the generation of reactive oxygen species (ROS) that are produced in mitochondria as by-products of cellular respiration. In healthy cells, the concentration of ROS is minimized by a system of biological antioxidants. However, heat shock changes the equilibrium between oxidative stress and antioxidant activity, that is, a rapid rise in temperature induces biophoton emission from ROS. Although the rate and intensity of biophoton emission was observed to increase in response to elevated temperatures, pretreatment at lower high temperatures inhibited photon emission at higher temperatures. Biophoton measurements are useful for observing and evaluating heat shock.     

IL-2 Regulates SEB Induced Toxic Shock Syndrome in BALB/c Mice

Background

Toxic Shock Syndrome (TSS) is characterized by fever, rash, hypotension, constitutional symptoms, and multi-organ involvement and is caused by Staphylococcus aureus enterotoxins such as Staphylococcal Enterotoxin B (SEB). SEB binds to the MHC-IIα chain and is recognized by the TCRβ chain of the Vβ8 TCR⁺ T cells. The binding of SEB to Vβ chain results in rapid activation of T cells and production of inflammatory cytokines, such as Interleukin-2 (IL-2), Interferon-γ and Tumor Necrosis Factor-α which mediate TSS. Although IL2 was originally identified as the T cell growth factor and was proposed to contribute to T cell differentiation, its role in TSS remains unexplored.

Methodology/Principal Findings

Mice were injected with D-Gal (25 mg/mouse). One hour after D-Galactosamine (D-Gal) injection each mouse was injected with SEB (20 µg/mouse. Mice were then observed for 72 hrs and death was recorded at different times. We tested Interleukin-12, IFNγ, and IL-2 deficient mice (IL-2^−/−), but only the IL-2 deficient mice were resistant to SEB induced toxic shock syndrome. More importantly reconstitution of IL-2 in IL-2 deficient mice restored the shock. Interestingly, SEB induced IL-2 production from T cells was dependent on p38MAPK activation in macrophages as inhibition of it in macrophages significantly inhibited IL-2 production from T cells.

Conclusion

This study shows the importance of IL -2 in TSS which has not been previously explored and it also shows that regulating macrophages function can regulate T cells and TSS.     

温度休克法诱导草履虫的同步分裂

运用细胞周期原理,采用温度休克法,对尾草履虫进行分裂周期同步化的研究,实验中草履虫经过3－5h的处理后,就能观察到大量不同阶段的无性生殖横分裂状态,并获得了大量处于分裂阶段的草履虫。运用这种技术取材容易,获取率稳定,可达61％,可为细胞生理学等领域的研究提供大量的同步分裂个体。     

温度休克法诱导草履虫的同步分裂

运用细胞周期原理,采用温度休克法,对尾草履虫进行分裂周期同步化的研究,实验中草履虫经过3～5 h的处理后,就能观察到大量不同阶段的无性生殖横分裂状态,并获得了大量处于分裂阶段的草履虫.运用这种技术取材容易,获取率稳定,可达61%,可为细胞生理学等领域的研究提供大量的同步分裂个体.     

Cold Shock Syndrome in Anacystis nidulans

The phenomenon of cold shock in Anacystis nidulans has been explored further in terms of loss of viability and immediate and subsequent metabolic effects. Cold shock was observed also in two closely related strains in which unsaturated fatty acid contents are also known to be low and temperature-dependent. Loss of viability was maximum for cells grown at temperatures above 40 C (<10⁻⁴ survivors after 5 min at 0 C) but became negligibly small for cells grown below 34 C. Development of the cold-sensitive condition after transfer 25 → 39 C was slow and comparable to rate of growth; development of the insensitive condition after transfer 39 → 25 C was rapid, implying rapid in situ alteration. An immediate metabolic effect, observed as a decrease in rate of photosynthetic O₂ evolution measured at growth temperature, was less severe than loss of viability. Continued light incubation under growth conditions led to slow decay in rate of O₂ evolution accompanied by loss of membrane chlorophyll. The multiple effects which comprise the cold shock syndrome appear to be membrane-related phenomena and thereby provide an experimental probe of normal membrane function.     

Systemic Lupus Erythematosus Syndrome Induced by Practolol

Three patients with angina pectoris treated with practolol in varying doses developed a syndrome of arthralgia, particularly of the small joints of the hands, rash, fever, a raised E.S.R., and positive tests for lupus erythematosus (L.E.) cells and antinuclear antibody. The syndrome responded partly to withdrawal of the drug, but steroids were required to produce adequate symptomatic improvement. These disease features suggest that this is an example of drug-induced systemic lupus erythematosus (S.L.E.). The impaired ability of lymphocytes from these patients to transform in vitro indicates a testable hypothesis for the pathogenesis of the syndrome.