In vivo inhibition of megakaryocyte and platelet production by platelet factor 4 in mice.

The in vivo effect of human platelet factor 4 (PF4) on murine megakaryocytopoiesis and thrombopoiesis was studied. Administration of PF4 induced a dose-dependent decrease in the numbers of megakaryocytes and their progenitor cells (CFU-MK), continuing for 1 week after the injection. However, the size of megakaryocytes and their colonies was not changed following PF4 injection. Platelet levels were significantly decreased at days 3-4. The number of CFU-GM was decreased at days 1-2. White blood cells and hemoglobin were unaffected by PF4. These data indicate that PF4 inhibits megakaryocyte and platelet production in vivo by acting on the early stage of megakaryocyte development.     

Proteolytic processing in a non-lysosomal compartment is required for transcytosis of protein-polylysine conjugates in cultured Madin-Darby canine kidney cells

The transcytosis of horseradish peroxidase, as well as its poly(L-lys) and poly(D-lys) thioether conjugates, was investigated in Strain I Madin-Darby canine kidney (MDCK) cell monolayers grown on 0.4 microns pore size polycarbonate membranes in Costar Transwells. The 3 types of HRP had almost identical rates of transport during the first 2 hr of incubation. However, a significant increase of basal-to-apical transport was detected beginning at 3 hr only in Transwells containing the poly(L-lys) conjugate. This increase was inhibited by colchicine (2 microM) and by the Bowman-Birk protease inhibitor (0.1 mg/ml), but not by NH4Cl (10 mM) or chloroquine (0.1 mM). The increase was abolished either by prior trypsinization of the conjugate or by incubation at 4 degrees C. Ultrafiltration studies indicated that the transcytosed poly(L-lys) conjugate was smaller in size than the original conjugate. These results indicate that the conjugate was processed during transcytosis in a non-lysosomal proteolytic compartment, where its poly(L-lys) moiety was selectively degraded, allowing active peroxidase to be released into the apical medium.     

银纹夜蛾的核型多角体病毒病

银纹夜蛾(Plusia agnata Staudinger)幼虫是大豆主要食叶害虫。在泰安地区,历年约占大豆害虫总发生量的70％以上;除大豆外,还为害甘蓝、白菜、棉麻等作物。 1979年6月,发现室内饲养的银纹夜蛾幼虫有倒挂死亡的虫体,经鉴定是一种核型多角体病毒病,现将其实验结果报道如下。     

家蚕卵裂核第一次分裂的方位观察

卵裂在胚胎学上有一定的规律,Wilson(1892)曾从几何学的角度,说明卵裂面对于卵轴或胚轴的位置关系,裂球对于正体位置关系的卵裂类型,主要取决于成胚原形质和卵黄的分配。家蚕卵的类型属于中黄卵,在卵黄膜内几乎全是卵黄集中分配的地方,只有在动物极的漏斗状范围内,卵黄分配稀少。卵的成熟分裂、受精和卵裂都开始在卵的动物极内(图1),然后引向植物极。     

Study of a possible structural relationship between thymopoietin and the facteur thymique serique

Background peptide chemistry, and the known 49-amino acid sequence of thymopoietin and the known 9-amino acid sequence of the facteur thymique serique (FTS) allowed the concept that Arg⁴⁹ of thymopoietin might be linked to Gln¹ of FTS in a new 58-amino acid peptide in tissue. Cleavage between Arg⁴⁹ and Gln⁵⁰ adjacent to the unique Lys⁴⁸-Arg⁴⁹ moiety could liberate thymopoietin and the [H-Gln¹]-FTS which could cyclize to FTS by the known reaction. In support of, rather than negating, this concept, synthetic FTS and the new dodecapeptide consisting of Val-Lys-Arg linked to the N-terminal of [H-Gln¹]-FTS showed comparable immune stimulating activity, $\text{in vivo}$; both peptides appeared more active than synthetic thymopoietin II.     

花尾榛鸡冬季活动区及社群行为

无线电遥测结果表明,长白山冬季花尾榛鸡的月活动区大小为22.5～6.52hm~2。11月至1月,随着天气变冷,花尾榛鸡的活动区面积明显减小(P<0.001)。冬季花尾榛鸡的日活动范围很小,平均466±127m~2。整个冬季花尾榛鸡的活动中心区出现阶段性改变。花角榛鸡对其活动区有一定的依赖性。花尾榛鸡冬季不存在明显的领域,出现集群行为,这与其栖息地食物丰富与抵御天敌有关。花尾榛鸡集群的组织结构是松散的,缺乏义务性,集群中的个体关系有亲疏,存在2只或2只以上个体组成的小组,同组个体之间的距离大多数情况在150～200m以内的联系范围内。推测花尾榛鸡集群时的活动区面积增大。     

Modeling influenza seasonality in the tropics and subtropics

Climate drivers such as humidity and temperature may play a key role in influenza seasonal transmission dynamics. Such a relationship has been well defined for temperate regions. However, to date no models capable of capturing the diverse seasonal pattern in tropical and subtropical climates exist. In addition, multiple influenza viruses could cocirculate and shape epidemic dynamics. Here we construct seven mechanistic epidemic models to test the effect of two major climate drivers (humidity and temperature) and multi-strain co-circulation on influenza transmission in Hong Kong, an influenza epidemic center located in the subtropics. Based on model fit to long-term influenza surveillance data from 1998 to 2018, we found that a simple model incorporating the effect of both humidity and temperature best recreated the influenza epidemic patterns observed in Hong Kong. The model quantifies a bimodal effect of absolute humidity on influenza transmission where both low and very high humidity levels facilitate transmission quadratically; the model also quantifies the monotonic but nonlinear relationship with temperature. In addition, model results suggest that, at the population level, a shorter immunity period can approximate the co-circulation of influenza virus (sub)types. The basic reproductive number R₀ estimated by the best-fit model is also consistent with laboratory influenza survival and transmission studies under various combinations of humidity and temperature levels. Overall, our study has developed a simple mechanistic model capable of quantifying the impact of climate drivers on influenza transmission in (sub)tropical regions. This model can be applied to improve influenza forecasting in the (sub)tropics in the future.