Hibernation and disuse osteoporosis.

In an attempt to determine 1) if disuse osteoporosis occurs naturally during hibernation and 2) if it can be induced by limb immobilization in active and hibernating ground squirrels, forty-six thirteenlined ground squirrels were divided into five experimental groups. Group one was the active control group (AC) (ten animals). Group two was the active immobilized (AI) group and was subjected to a unilateral sciatic nerve section (ten animals). Group three was the hibernating control group and was allowed to hibernate undisturbed for 30 days (HC) (ten animals). The fourth group was subjected to a unilateral sciatic nerve section and allowed to hibernate for 30 days; this was the hibernating immobilized group (HI). The fifth group of six animals received the identical treatment as the (HI) group but was allowed to hibernate for 150 days.The following measurements were taken: Gastrocnemius-soleus mass, body mass, tibia-fibula weight, total tibia-fibula calcium and phosphorus. In addition, the femur was observed histologically for the enlarged lacunae typical of osteoporotic bone. Statistical analysis was accomplished with the Wilcoxan sign rank test.The data were interpreted to mean: 1) Disuse osteoporosis can be induced in active ground squirrels, 2) disue osteoporosis is not evident nor can it be induced by limb immobilization during 30 days of hibernation and 3) limb immobilization did not result in significant disuse osteoporosis following 150 days of hibernation. Only a few enlarged lacunae were evident after 150 days of hibernation.     

朱砂叶螨越冬的研究

朱砂叶螨(Tetranychus cinnabarinus)原多混同于二斑叶螨(T.urticae),为世界性害螨,在我国严重危害棉花、瓜、豆、茄果类蔬菜及许多观赏植物。叶螨科叶螨属的很多种类以滞育态雌成螨     

Site-specific recombination in the immune system.

Site-specific DNA recombination has been identified in a wide variety of biological systems. In vertebrates, however, the only identified use of this genetic device is in the immune system. Here it plays a critical role in generating a diverse repertoire of surface receptors to intercept invading microbes and parasites. The mechanism and orchestration of this reaction are intriguing and are relevant to a broad array of related biological and biomedical issues.     

Neonatal exposure to UVR alters skin immune system development, and suppresses immunity in adulthood

Neonates have a developing immune response, with a predisposition towards induction of tolerance. As the immune system develops, immunity rather than tolerance is induced, with this development of immunity occurring in response to external factors such as the environment. As ultraviolet radiation (UVR) suppresses immunity, it is likely that the effect of UVR on the neonatal immune system would be augmentation of the suppressive response. In support, childhood exposure to UVR has been linked with an increased incidence of melanoma; consistent with an increase in suppression. To address this, phenotypic and functional immune system studies were undertaken at 8 weeks after one single exposure of solar-simulated UVR to mice, when mice had reached adulthood. Subtle changes were observed in cell populations resident in the skin-draining lymph nodes (LNs) and there also appeared to be a subtle, but not statistically significant, increase in the production of interleukin-10 and interferon-γ. Importantly, these changes also corresponded with significant suppression of the contact hypersensitivity response in irradiated mice compared with their control counterparts. This suppression was apparent when antigen sensitisation occurred during the neonatal or adult period, and thus did not appear to be analogous to UVR-induced suppression in adults. Although the percentage of T regulatory cells was increased in the skin-draining LNs, they were induced in a different manner to those induced following adult UVR exposure, with no increase in function on a per-cell basis. It therefore appears that one single neonatal exposure to UVR alters development of the immune system, leading to long-term implications for induction of immunity.     

Neonatal immune challenge alters reproductive development in the female rat

This article is part of a Special Issue "Neuroendocrine-Immune Axis in Health and Disease." Neonatal lipopolysaccharide (LPS) exposure alters neuroendocrine, immune and behavioural responses in adult rats. Recent findings indicate that neonatal LPS treatment may have a more pronounced effect on the mating behaviours of females compared to males. The current study further explored the impact of neonatal inflammation on reproductive development in the female rat. Wistar rats were administered LPS (0.05mg/kg, i.p.) or saline (equivolume) on postnatal days (PNDs) 3 and 5. The immediate effect of treatment was assessed on plasma corticosterone and tyrosine hydroxylase (TH) phosphorylation in the adrenal medulla. Weight gain and vaginal opening were recorded, and oestrous cyclicity was monitored post-puberty and in late adulthood. Blood and ovaries were collected throughout development to assess HPA and HPG hormones and to examine ovarian morphology. Reproductive success in the first (F1) generation and reproductive development in the second (F2) generation were also assessed. Neonatal LPS exposure resulted in increased TH phosphorylation in the neonatal adrenals. LPS treatment increased the corticosterone concentrations of females as juveniles, adolescents and adults, and reduced FSH in adolescence. Increased catch-up growth was evident in LPS-treated females, prompting earlier onset of puberty. Diminished follicular reserve was observed in neonatally LPS-treated females along with the advanced reproductive senescence. While fertility rates were not compromised, higher mortality and morbidity were observed in litters born to LPS-treated mothers. Female offspring of LPS-treated mothers displayed increased corticosterone on PND 14, increased catch-up growth and delayed emergence of the first oestrous cycle. No differences in any of the parameters assessed were observed in F2 males. These data suggest that neonatal immunological challenge has a profound impact on the female reproductive development, via the alteration of metabolic and neuroendocrine factors which regulate sexual maturation. Evidence of altered development in the female, but not male offspring of LPS-treated dams suggests increased susceptibility of females to the deleterious effects of neonatal immunological stress and its possible transferability to a subsequent generation.     

Life-or-death fate in the adaptive immune system.

The tissue homeostasis is essentially realized through a precise control of cellular proliferation and death. The constant balance between expansion and contraction of different cell populations is a critical hallmark of the mammalian adaptive immune system. Immune-competent cells have to confront the survival-or-demise dilemma in primis during ontogenesis and, thereafter, in their mature life in order to maintain homeostasis, since the cellular proliferation occurring during the immune response must be counterbalanced by programmed death as the immune reaction attenuates. The programmed cell death is mainly realized through apoptosis. Perturbations in precise control of lymphocyte life-or-death balance may lead to pathological processes, such as immunodeficiencies, autoimmunity or lymphoproliferative disorders. The life-or-death fate in the human adaptive immune system is reviewed and discussed.