The molecular and cellular actions of three classes of abused drugs--opiates, psychostimulants, and ethanol--are reviewed in the context of behavioral studies of drug dependence. The immediate effects of drugs are compared to those observed after long-term exposure. A neurobiological basis for drug dependence is proposed from the linkage between the cellular and behavioral effects of these drugs.

https://science.sciencemag.org/content/sci/242/4879/715.full.pdf

Cellular and molecular mechanisms of drug dependence.

Critical Care Medicine : Organizing and Staffing Intensive Care Units

Autologous bone grafts harvested from the iliac crest are commonly used in reconstructive orthopaedic surgery. Autologous bone is used to help promote bone healing in fractures and to provide structural support for reconstructive surgery. The results of autologous bone grafting are more predictable than the use of xenografts, cadaveric allografts, or synthetic bone substitutes because autologous bone grafts provide osteoinductive and osteoconductive properties, are not immunogenic, and are usually well incorporated into the graft site. In a retrospective review of 414 consecutive cases of iliac crest bone graft procedures performed at Brooke Army Medical Center from 1983 to 1993, 41 (10%) minor and 24 (5.8%) major complications were identified. Minor complications included superficial infections, superficial seromas, and minor hematomas. Major complications included herniation of abdominal contents through massive bone graft donor sites, vascular injuries, deep infections at the donor site, neurologic injuries, deep hematoma formation requiring surgical intervention, and iliac wing fractures. Harvesting of iliac crest bone graft can be associated with significant morbidity. However, with adequate preoperative planning and proper surgical technique, the incidence of these complications can be reduced.

Complications of Iliac Crest Bone Graft Harvesting

Summary Cerebellar ataxias with autosomal dominant transmission are rare, but identification of the associated genes has provided insight into the mechanisms that could underlie other forms of genetic or non-genetic ataxias. In many instances, the phenotype is not restricted to cerebellar dysfunction but includes complex multisystemic neurological deficits. The designation of the loci, SCA for spinocerebellar ataxia, indicates the involvement of at least two systems: the spinal cord and the cerebellum. 11 of 18 known genes are caused by repeat expansions in the corresponding proteins, sharing the same mutational mechanism. All other SCAs are caused by either conventional mutations or large rearrangements in genes with different functions, including glutamate signalling (SCA5/ SPTBN2 ) and calcium signalling (SCA15/16/ ITPR1 ), channel function (SCA13/ KCNC3 , SCA14/ PRKCG , SCA27/ FGF14 ), tau regulation (SCA11/ TTBK2 ), and mitochondrial activity (SCA28/ AFG3L2 ) or RNA alteration (SCA31/ BEAN-TK2 ). The diversity of underlying mechanisms that give rise to the dominant cerebellar ataxias need to be taken into account to identify therapeutic targets.

Autosomal dominant cerebellar ataxias: polyglutamine expansions and beyond

Mitochondrial optic neuropathies – Disease mechanisms and therapeutic strategies

"Tennis thumb" tendinitis with calcification in flexor policies longus.

MONDOR'S DISEASE: A Superficial Phlebitis of the Breast

A barber's interdigital pilonidal sinus.

Rupture of the spleen, and thrombocytopenia, in glandular fever.

Congenitally short frenula of upper lip and tongue.

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