The light microscopic localization of substance P- and somatostatin-like immunoreactive cells in the larval tiger salamander retina

Summary Light microscopic immunocytochemistry was utilized to localize the populations of substance P (SP)- and somatostatin (SOM)-like immunoreactive cells in the larval tiger salamander retina. Of 104 SP-immunostained cells observed, 82% were Type 1 amacrine cells. Another 8% of the SP-cells were classified as Type 2 amacrine cells, while 10% of the SP-cells had their cell bodies located in the ganglion cell layer and were designated as displaced amacrine cells. Each type of SP-like immunoreactive cell was observed in the central and peripheral retina. SP-immunopositive processes were observed in the inner plexiform layer as a sparse plexus in sublamina 1 and as a denser network of fibers in sublamina 5. Seventy-eight percent of the 110 somatostatin-immunopositive cells observed were designated as Type 1 amacrine cells. Another 12% of SOM-cells were classified as displaced amacrine cells, while only two SOM-immunopositive Type 2 amacrine cells were observed. Nine percent of the SOM-cells were designated as interplexiform cells, based on their giving rise to processes distributing in the outer plexiform layer as well as processes ramifying in the inner plexiform layer. Each type of SOM-immunoreactive cell was observed in the central and peripheral retina, with the exception of the Type 2 amacrine cells, whose somas were only found in the central retina. Lastly, SOM-immunopositive processes in the inner plexiform layer appeared as a fine plexus in sublamina 1 and as a somewhat denser network of fibers in sublamina 5.     

脑啡肽与生长抑素在鸡视网膜无长突细胞共存的免疫组织化学研究

本文介绍用免疫组织化学的单标和双标技术研究脑啡肽(ENK)和生长抑素(SOM)在鸡视网膜无长突细胞的定位和共存。单标的实验结果表明,一些SOM免疫反应阳性无长突细胞的形态、胞体在内核层的位置及其突起在内网层的分支式样与某些ENK免疫反应阳性无长突细胞相似,虽然其突起在内网层的第3、4亚层形成的丛网不象ENK免疫反应阳性突起那样丛密,在内网层的第5亚层也未见SOM免疫阳性突起。双标的实验结果表明,一些无长突细胞显示ENK和SOM两种免疫阳性反应,而另一些无长突细胞分别只显示ENK或SOM阳性免疫反应。文中还对视网膜神经多肽间或与经典神经递质的共存进行了讨论。     

Partial destruction of Borrelia burgdorferi within ticks that engorged on OspE- or OspF-immunized mice.

We determined whether Borrelia burgdorferi outer surface proteins (Osps) E and F could elicit immune responses useful for a Lyme disease vaccine. Thirty days after challenge with B. burgdorferi, mice produced antibodies to OspE but not OspF, whereas antibodies to OspF were present in sera of mice obtained 90 days after infection. Examination of sera from patients with Lyme disease revealed antibodies to OspF in a small number (14%) of early-stage disease patients but in a majority (58%) of patients with late-stage disease, while antibodies to OspE were rarely detected in patients. Mice immunized with recombinant OspE or OspF produced high titers of antibodies to OspE or OspF, respectively. OspF-immunized mice were partially protected from both intradermal syringe challenge and tick-mediated transmission of B. burgdorferi while vaccination with OspE did not confer immunity. B. burgdorferi organisms were, however, substantially destroyed within ticks that engorged on either OspE- (75% reduction in the number of spirochetes within the ticks, compared with controls) or OspF (90% reduction in the number of spirochetes within the ticks)-immunized mice.     

Talo-patello-scaphoid osteolysis,synovitis, and short fourth metacarpals in sisters: a new syndrome?

Osteolysis syndromes are characterized by resorption of affected bones with associated swelling and pain. Various forms of multicentric osteolysis syndromes including autosomal dominant and recessive carpal-tarsal osteolysis, Torg, Fran?ois, Whyte-Hemingway, Hajdu-Cheney, Winchester, and other forms have been described. Most present in pre-school years with extensive involvement and destruction of multiple bones. We present a sister-pair, both of whom presented in early teenage, i.e., 13 and 15.5 years, respectively, with bilateral ankle, knee, and later, wrist pain. Radiological examination revealed bilateral osteolysis of tali, scaphoids, and patellae, and short fourth metacarpals in both sisters. Further investigation revealed absence of renal involvement, a normal excretion of amino acids, mucopolysaccharides and oligosaccharides, and presence of chronic synovitis in both sisters. Both parents and a younger brother were without radiographic or clinical evidence of the disease and there was no history of consanguinity. Thus, our sister-pair presented with the same carpal and tarsal bone involvement at a much later age, with evidence of chronic synovitis, along with short fourth metacarpals (brachydactyly type E changes) and without renal disease, suggesting a new syndrome with probable autosomal recessive inheritance.     

Cooperation between the Cdk inhibitors p27KIP1 and p57KIP2 in the control of tissue growth and development

Cell cycle exit is required for terminal differentiation of many cell types. The retinoblastoma protein Rb has been implicated both in cell cycle exit and differentiation in several tissues. Rb is negatively regulated by cyclin-dependent kinases (Cdks). The main effectors that down-regulate Cdk activity to activate Rb are not known in the lens or other tissues. In this study, using multiple mutant mice, we show that the Cdk inhibitors p27^KIP1 and p57^KIP2 function redundantly to control cell cycle exit and differentiation of lens fiber cells and placental trophoblasts. These studies demonstrate that p27^KIP1 and p57^KIP2 are critical terminal effectors of signal transduction pathways that control cell differentiation.     

Cardiac Myxoma: Histochemical and Ultrastructural Localization of Glycosaminoglycans and Proteoglycans

A recurrent cardiac myxoma is examined histochemical ly at the ultrastructural level. By routine electron microscopy the stellate “myxoma” cell exhibits features suggestive of a secretory function in synthesis of its myxoid stroma. Spicer's high iron diamine (HID), which stains specifically for sulfated glycoconjugates, is utilized for intracellular localization of glycosaminoglycans. HID-positive reactive sites are localized within the Golgi-derived vacuoles and secretory granules of the myxoma cells. No staining is obtained with other cytoplasmic organelles except rare secondary lyso-somes. Although colloidal iron is less specific, both intracellular and extracellular positive reactive sites are observed. With ruthenium red staining the proteoglycans in the extracellular stroma can be visualized as numerous positively stained, polygonal 250-500 A matrix granules with faint filamentous projections. Positive intracellular ruthenium red-stained granules are also observed within the Golgi-derived vacuoles. The alcianophilia of the myxoid stroma with Alcian blue is almost completely abolished by prior treatment with bovine testicular hyaluronidase but is unaffected by leech hyaluronidase, indicating chondroitin sulfates A and/or C, not hyaluronic acid, as the major biochemical constituents of the stroma and the observed extracellular matrix granules. The above findings provide cytochemical evidence of intracellular synthesis of sulfated glycosaminoglycans and proteoglycans of the myxoma cell and its active participation in production of its stroma.     

Recurrent and novel mutations of GCDH gene in Chinese glutaric acidemia type I families

Glutaric acidemia type I is caused by mutations of the glutaryl-CoA dehydrogenase (GCDH) gene resulting in loss of GCDH enzyme activity. Patients present with progressive dystonia and lesions in basal ganglia. Dietary treatment, when instituted from the early neonatal period, markedly reduces dystonia and morbidity. Early diagnosis and prenatal diagnosis will be facilitated by knowledge of locally prevalent GCDH mutations. Several common GCDH mutations have been found in different ethnic groups. GCDH mutations were studied in 5 Chinese glutaric acidemia type I families. We detected two novel recurrent mutations (A219T and IVS10-2A>C) which were found in two unrelated families. An asymptomatic carrier of IVS10-2A>C was also found on screening of 120 individuals. Other mutations were identified, including two other novel (R386G & IVS3+1G>A) and two known mutations (G178R & R355H). Fibroblasts from patients carrying the novel mutations were confirmed to be deficient for GCDH activity. This is the first report of GCDH mutations describing recurrent mutations in Chinese patients. The carrier rate of IVS10-2A>C may be particularly high in Chinese.