The Drosophila caspases Strica and Dronc function redundantly in programmed cell death during oogenesis.

Programmed cell death (PCD) in the Drosophila ovary occurs either during mid-oogenesis, resulting in degeneration of the entire egg chamber or during late oogenesis, to facilitate the development of the oocyte. PCD during oogenesis is regulated by mechanisms different from those that control cell death in other Drosophila tissues. We have analyzed the role of caspases in PCD of the female germline by examining caspase mutants and overexpressing caspase inhibitors. Imprecise P-element excision was used to generate mutants of the initiator caspase strica. While null mutants of strica or another initiator caspase, dronc, display no ovary phenotype, we find that strica exhibits redundancy with dronc, during both mid- and late oogenesis. Ovaries of double mutants contain defective mid-stage egg chambers similar to those reported previously in dcp-1 mutants, and mature egg chambers with persisting nurse cell nuclei. In addition, the effector caspases drice and dcp-1 also display redundant functions during late oogenesis, resulting in persisting nurse cell nuclei. These findings indicate that caspases are required for nurse cell death during mid-oogenesis, and participate in developmental nurse cell death during late oogenesis. This reveals a novel pathway of cell death in the ovary that utilizes strica, dronc, dcp-1 and drice, and importantly illustrates strong redundancy among the caspases.

Programmed cell death in the germline.

In many organisms, programmed cell death of germ cells is required for normal development. This often occurs through highly conserved events including the transfer of vital cellular material to the growing gametes following death of neighboring cells. Germline cell death also plays a role in such diverse processes as removal of abnormal or superfluous cells at certain checkpoints, establishment of caste differentiation, and individualization of gametes. This review focuses on the cell death events that occur during gametogenesis in both vertebrates and invertebrates. It also examines the signals and machinery that initiate and carry out these germ cell deaths.

Atraumatic osteochondral fracture and osteoarthritis in a collegiate volleyball player: a case report.

OBJECTIVE: To present the case of a collegiate athlete with an atraumatic osteochondral fracture influenced by the presence of osteoarthritis. BACKGROUND: Osteochondral fractures are fairly common occurrences in athletes, although it can be difficult to recognize such an injury in the absence of a traumatic event. Osteoarthritis is 1 condition that can increase an athlete's susceptibility to an atraumatic osteochondral fracture. However, because of the atraumatic nature of the injury, the possibility of an osteochondral fracture may be overlooked. DIFFERENTIAL DIAGNOSIS: Meniscal damage, osteochondritis dissecans, patellofemoral disorders. TREATMENT: The osteochondral fragment was surgically removed, and fibrous growth was encouraged by drilling and laser smoothing. UNIQUENESS: Osteochondral fractures are usually associated with some type of traumatic mechanism, such as a rotational and compressive force. Also, osteoarthritis is not common in young collegiate athletes. However, this 20-year-old volleyball player had no apparent injury and lacked the usual signs and symptoms (eg, locking, giving way, crepitus, loss of range of motion) associated with an osteochondral fracture. The athlete's susceptibility to an osteochondral fracture was increased by the presence of osteoarthritis. CONCLUSIONS: The athletic trainer should consider the possibility of an osteochondral fracture in an athlete with persistent effusion and pain in the absence of a traumatic mechanism of injury.

Arginine vasopressin stimulates protein synthesis but not proliferation of cultured vascular endothelial cells.

We previously showed that rat and cow blood vessels contain arginine vasopressin (AVP) of local origin. In the present study, to investigate potential roles for this locally produced peptide, we examined the effects of AVP on growth of cultured vascular endothelial and smooth muscle cells (EC, SMC). Treatment of cultured bovine aortic endothelial (BAE), murine cerebral microvascular endothelial (MME), or murine cerebral microvascular smooth muscle (MMSM) cells with AVP produced dose-dependent increases in total protein content with maximum increases of 11, 46, and 33% over vehicle-treated controls, respectively. AVP also dose-dependently increased new protein synthesis, as reflected by [3H]leucine incorporation into BAE and MME cell protein, with maximal increases of 34 and 24%, respectively. In addition, the AVP-stimulated increase in protein synthesis could be significantly attenuated in both BAE and MME cells by simultaneous addition of a specific AVP V1 receptor antagonist. In contrast, AVP did not affect total cell number or DNA synthesis, as reflected by [3H]thymidine incorporation, in any cell type. Neither was cell size, as measured by forward light scatter with a fluorescence-activated cell sorter (FACS), changed by treatment with AVP. However, the density of individual cells, as measured by orthogonal light scatter with FACS, was increased by AVP. These data demonstrate that AVP stimulates protein synthesis but not proliferation of cultured vascular EC and SMC and suggest that locally produced AVP may function as a growth factor for these cells.

Design features of a biotechnology laboratory environment.

This article addresses those aspects of laboratory building design that pertain to life safety, industrial hygiene, and accident prevention. The manner by which health and safety professionals can participate in planning facilities is emphasized.