Objective To observe the efficacy of liposomal doxorubicin combined with cyclophosphamide, vincristine and prednisone in the treatment of refractory Non-Hodgkin’s lymphoma.Methods Liposomal doxorubicin (40mg/m2) was given by intravenous drip in the 1st day. Cyclophosphamide (750mg/m2) was given by intravenous injection in the 1st day. Vincristine (2mg) was given by intravenous injection in the 1st day. Prednisone (100mg/m2) was given orally from the 1st to the 5th day. A cycle was repeated every 3 to 4 weeks. Every patient took at least 2 cycles of the regimen.Results A total of 13 patients were assessed in the group. Among them, 7 were completely release (53.8), 4 were partially release (30.67) and 2 remained the same (15.35). The B symptom of 7 patients in the 9 with that disappeared, and that of the other 2 patients was improved obviously. The most common adverse effects were slight gastrointestinal reactions and the grade Ⅲ bone marrow suppression in a few patients. Conclusion The regimen of liposomal doxorubicin combined with cyclophosphamide, vincristine and prednisone is effective in the treatment of refractory Non-Hodgkin’s lymphoma with tolerable toxicity. It may be a salvage chemotherapeutic regimen deserving further study.

Previous genetic fate-mapping studies have indicated that embryonic glial fibrillary acidic protein-positive (GFAP) cells are multifunctional progenitor/neural stem cells that can produce astrocytes as well as neurons and oligodendrocytes throughout the adult mouse central nervous system (CNS). However, emerging evidence from recent studies indicates that GFAP cells adopt different cell fates and generate different cell types in different regions. Moreover, the fate of GFAP cells in the young adult mouse CNS is not well understood. In the present study, hGFAP-Cre/R26R transgenic mice were used to investigate the lineage of embryonic GFAP cells in the young adult mouse CNS. At postnatal day 21, we found that GFAP cells mainly generated NeuN neurons in the cerebral cortex (both ventral and dorsal), hippocampus, and cerebellum. Strangely, these cells were negative for the Purkinje cell marker calbindin in the cerebellum and the neuronal marker NeuN in the thalamus. Thus, contrary to previous studies, our genetic fate-mapping revealed that the cell fate of embryonic GFAP cells at the young adult stage is significantly different from that at the adult stage.
Animals ; Astrocytes ; cytology ; metabolism ; Brain ; cytology ; growth & development ; metabolism ; Calbindins ; metabolism ; Glial Fibrillary Acidic Protein ; metabolism ; Mice ; Mice, Transgenic ; Nerve Tissue Proteins ; metabolism ; Neural Stem Cells ; cytology ; metabolism ; Neurons ; cytology ; metabolism ; Nuclear Proteins ; metabolism

Objective:To analyze the clinical characteristics and gene detection methods of pseudohypertrophic muscular dystrophy, and to provide evidence for gene diagnosis and genetic counseling.Methods:Ten patients with pseudohypertrophic muscular dystrophy diagnosed clinically in the First Affiliated Hospital of Henan University of Science and Technology from March 2018 to March 2019 were selected. The clinical features were analyzed and multiplex ligation probe amplification technique (MLPA) was detected, and exon sequencing was performed in some patients.Results:Ten patients with clinical diagnosis were diagnosed as pseudohypertrophic muscular dystrophy in 9 cases and limb band muscular atrophy in 1 case. The ratio of male to female was 8∶1 in 9 cases. Exon region large deletion of Duchenne muscular dystrophy (DMD) gene was found in 6 cases, and point new mutation in 3 cases. The three possible new mutations of DMD gene were c. 10222delA、c.5697dupA、c.676_678del.Conclusions:Patients with typical symptoms but inconsistent with X-linked recessive inheritance still need DMD genetic detecting; patients with negative MLPA testing need full exon sequencing; patients with mental retardation should pay attention to avoid misdiagnosis.

The main lysosomal protease cathepsin D (cathD) is essential for maintaining tissue homeostasis via its degradative function, and its loss leads to ceroid accumulation in the mammalian nervous system, which results in progressive neurodegeneration. Increasing evidence implies non-proteolytic roles of cathD in regulating various biological processes such as apoptosis, cell proliferation, and migration. Along these lines, we here showed that cathD is required for modulating dendritic architecture in the nervous system independent of its traditional degradative function. Upon cathD depletion, class I and class III arborization (da) neurons in Drosophila larvae exhibited aberrant dendritic morphology, including over-branching, aberrant turning, and elongation defects. Re-introduction of wild-type cathD or its proteolytically-inactive mutant dramatically abolished these morphological defects. Moreover, cathD knockdown also led to dendritic defects in the adult mushroom bodies, suggesting that cathD-mediated processes are required in both the peripheral and central nervous systems. Taken together, our results demonstrate a critical role of cathD in shaping dendritic architecture independent of its proteolytic function.

The laterodorsal tegmentum (LDT) is a brain structure involved in distinct behaviors including arousal, reward, and innate fear. How environmental stimuli and top-down control from high-order sensory and limbic cortical areas converge and coordinate in this region to modulate diverse behavioral outputs remains unclear. Using a modified rabies virus, we applied monosynaptic retrograde tracing to the whole brain to examine the LDT cell type specific upstream nuclei. The LDT received very strong midbrain and hindbrain afferents and moderate cortical and hypothalamic innervation but weak connections to the thalamus. The main projection neurons from cortical areas were restricted to the limbic lobe, including the ventral orbital cortex (VO), prelimbic, and cingulate cortices. Although different cell populations received qualitatively similar inputs, primarily via afferents from the periaqueductal gray area, superior colliculus, and the LDT itself, parvalbumin-positive (PV) GABAergic cells received preferential projections from local LDT neurons. With regard to the different subtypes of GABAergic cells, a considerable number of nuclei, including those of the ventral tegmental area, central amygdaloid nucleus, and VO, made significantly greater inputs to somatostatin-positive cells than to PV cells. Diverse inputs to the LDT on a system-wide level were revealed.