Treatment of acute diarrheal disease in infants (author's transl)]

In the treatment of acute diarrheal disease in infants reinstituting the normal intestinal homeostasis is of primary importance. Prompt rehydration should be accomplished with a well balanced glucose electrolyte solution by parenteral or oral route. From a diet, given after rehydration, lactose and long chain fatty acids must be eliminated. Antibiotics, cholestyramine or elemental diets are to be reserved for special situations.     

Cross-species immunity following immunization with a circumsporozoite protein-based vaccine for malaria

Malaria continues to be a major public health concern, and there are concerted efforts to eliminate it. The quest for a vaccine remains a top priority, and vaccines based on the circumsporozoite protein (CSP) are among the lead candidates, with the RTS,S vaccine currently undergoing phase 3 testing in Africa. Previous studies have reported anti-CSP antibody-mediated enhancement of in vitro invasion of homologous sporozoites. This effect has been shown to be concentration dependent; high-level antibodies are inhibitory, whereas low-level antibodies lead to enhancement of invasion. Nondominant shared epitopes may lead to the generation of low titers of cross-reactive antibodies that may prove to be detrimental. We report cross-species recognition of Plasmodium falciparum and Plasmodium berghei sporozoites by anti-Plasmodium vivax CSP serum samples. In addition, we report that vaccination of mice with VMP001, a P. vivax CSP vaccine candidate, reduces, not enhances, P. berghei infection in mice.     

Neutropenia as side effect of azlocillin in an infant (author's transl)

The authors report on a case of severe neutropenia in an infant treated with azlocillin. This case fits well into the series of wellknown reports on hematologic side effects of other semisynthetic penicillins, with regard to the onset of symptomatics, clinical side effects, and full reversibility.     

Newcastle disease outbreaks in Kazakhstan and Kyrgyzstan during 1998, 2000, 2001, 2003, 2004, and 2005 were caused by viruses of the genotypes VIIb and VIId

Newcastle disease virus (NDV) infects domesticated and wild birds throughout the world, and infections with virulent NDV strains continue to cause disease outbreaks in poultry and wild birds. To assess the evolutionary characteristics of 28 NDV strains isolated from chickens in Kazakhstan and Kyrgyzstan during 1998, 2000, 2001, 2003, 2004, and 2005, we investigated the phylogenetic relationships among these viruses and viruses described previously. For genotyping, fusion (F) gene phylogenetic analysis (nucleotide number 47–421) was performed using sequences of Kazakhstanian and Kyrgyzstanian isolates as compared to sequences of selected NDV strains from GenBank. Phylogenetic analysis demonstrated that the 14 newly characterized strains from years 1998 to 2001 belong to the NDV genotype VIIb, whereas the 14 strains isolated during 2003–2005 were of genotype VIId. All strains possessed a virulent fusion protein cleavage site (R-R-Q-R/K-R-F) and had intracerebral pathogenicity indexes in day-old chickens that ranged from 1.05 to 1.87, both properties typical of NDV strains classified in the mesogenic or velogenic pathotype.     

Accumulation of memory T cells from childhood to old age: central and effector memory cells in CD4(+) versus effector memory and terminally differentiated memory cells in CD8(+) compartment

Memory T cells can be classified as central memory (T(CM), CD45RA(neg)CCR7(+)), effector memory (T(EM), CD45RA(neg)CCR7(neg)), and terminally differentiated cells (T(TD), CD45RA(+)CCR7(neg)) with different homing and effector capacities. In 101 healthy subjects aged from 5 to 96 years, distinct dynamics were evidenced between circulating CD4(+) and CD8(+) T cell populations. Naive CD4(+) and CD8(+) T cells decreased linearly with age, CD8(+) twice more rapidly. Memory cells outnumbered naive cells on average at 37.4 in the CD4(+) and 29.5 years of age in the CD8(+) pool. CD4(+) T(CM) and T(EM) cells were positively correlated and increased linearly at a similar rate with age, while CD4(+) T(TD) remained rare. CD8(+) T(EM) and T(TD) accumulated linearly with age, while T(CM) increased only slightly, and each memory subset was negatively correlated to the two others. Almost all CD8(+) T(TD) and some CD8(+) T(EM) had lost CD28 expression. Despite different dynamics, each individual CD4(+) naive and memory subset was correlated to the synonymous CD8(+) subset. Half of the subjects aged 65 years or older were characterized by extremely reduced CD8(+) naive and increased CD8(+) T(TD) cell counts, which could indicate an acceleration of the decay of the immune system from this age onward.     

The impact of dapagliflozin on glucose excursions related to early proatherogenic derangement in the aortic wall

Introduction

Cardiovascular risk in the course of diabetes depends greatly on glycemic variability which is even more significant than chronic hyperglycemia. Optimal management of diabetes involves a multidisciplinary approach focused in particular on decreasing the risk of atherosclerosis. Therefore, our purpose was to evaluate the impact of dapagliflozin on glucose excursions and related proatherogenic changes in the aortic wall.

Tumorigenic effects mediated in the avian embryo by one or more oncogenes associated with v-myc.

We have previously shown that introduction of the v-myc oncogene in chick or quail embryos at E3 induces rapidly growing heart rhabdomyomas. We now report that a retrovirus containing one or two other oncogenes induces additional pathologies specified by the v-myc-associated oncogene. The v-mil/myc combination introduced at E3 induces, in addition to heart rhabdomyomas, tumors of proliferating cells aggregated onto the luminal aspect of vessels in both chick and quail embryos. In the quail these cells react positively with the quail-specific mAb QH1, which recognizes endothelial and most hemopoietic cells, while chick intravascular cells do not react with the chick-specific mAb VIA2 that recognizes hemopoietic cells. Thus the v-mil/myc tumors appear to be of endothelial origin. The v-myb-ets/myc combination injected at E3 induces cardiorhabdomyomas and aggressive VIA2-positive hemopoietic tumors in chick embryos, but only the v-myc-induced cardiorhabdomyomas in quail embryos. When injected into hatched animals, v-myc alone transforms hemopoietic and perhaps endothelial cells, but not cardiac cells. Thus the developmental stage at which a cell type can be transformed by v-myc and another associated oncogene depends on as yet undefined species-specific factors. More importantly, several examples of oncogene cooperation in vivo are adduced by these experiments. The type of cell transformed is specified by the viral oncogene combination.