The Latina Breast Cancer Control Study, year one: factors predicting screening mammography utilization by urban Latina women in Massachusetts

The mechanisms underlying secondary or delayed cell death following traumatic brain injury (TBI) are poorly understood. Recent evidence from experimental models of TBI suggest that diffuse and widespread neuronal damage and loss is progressive and prolonged for months to years after the initial insult in selectively vulnerable regions of the cortex, hippocampus, thalamus, striatum, and subcortical nuclei. The development of new neuropathological and molecular techniques has generated new insights into the cellular and molecular sequelae of brain trauma. This paper will review the literature suggesting that alterations in intracellular calcium with resulting changes in gene expression, activation of reactive oxygen species (ROS), activation of intracellular proteases (calpains), expression of neurotrophic factors, and activation of cell death genes (apoptosis) may play a role in mediating delayed cell death after trauma. Recent data suggesting that TBI should be considered as both an inflammatory and/or a neurodegenerative disease is also presented. Further research concerning the complex molecular and neuropathological cascades following brain trauma should be conducted, as novel therapeutic strategies continue to be developed.     

LGMD 2E in Tunisia is caused by a homozygous missense mutation in beta-sarcoglycan exon 3

Four of the currently recognized autosomal recessive limb-girdle muscular dystrophies (LGMD type 2C-F) are caused by mutations in the genes encoding components of the sarcoglycan complex. LGMD 2C, caused by mutations in gamma-sarcoglycan, is prevalent in northern Africa, especially in Tunisia, where this type of muscular dystrophy was originally described. Although the disease initially was assumed to be genetically homogeneous in this region, linkage to the alpha-sarcoglycan locus (LGMD 2D) has also been found. We have now identified the first Tunisian family with beta-sarcoglycanopathy (LGMD 2E), further adding to the genetic heterogeneity of autosomal recessive LGMD in this population. Direct sequencing of the beta-sarcoglycan gene revealed a homozygous mutation (G272-->T, Arg91Leu) in exon 3. This change affects the same arginine residue in the immediate extracellular domain of the protein that was mutated to a proline (G272-->C, Arg91Pro) in a Brazilian family with a severe form of the disease. Immunohistochemical analysis for the sarcoglycan complex demonstrates absence of the known components of the complex in both of these families. We postulate that the immediate extracellular domain of beta-sarcoglycan may be important for the assembly and/or maintenance of this complex, potentially mediated by disulfide-bond formation to another sarcoglycan via the single cysteine residue in that domain.     

Follow-up of argon laser trabeculoplasty: is a day-one postoperative IOP check necessary?

BACKGROUND AND OBJECTIVES: To evaluate the benefit of measuring the intraocular pressure (IOP) on the first postoperative day after argon laser trabeculoplasty (ALT). PATIENTS AND METHODS: We retrospectively reviewed 407 ALT procedures with perioperative apraclonidine performed on 226 patients between January 1991 and December 1993. Data analyzed included type of glaucoma, extent of treatment, whether the procedure was initial or repeat, laser parameters, and IOP preoperatively and at 1 hour, 1 day, and 1 month postoperatively. RESULTS: The percentage of patients with an IOP rise of greater than 3 mm Hg at 1 hour, 1 day, and 1 month following ALT was 11.3%, 4.2%, and 5.2% respectively. The incidence of IOP elevations greater than 10 mm Hg was 2.2%, 1.0%, and 1.5% at 1 hour, 1 day and 1 month, respectively. Of 17 cases with an IOP elevation greater than 3 mm Hg at 1 day, four eventually required a trabeculectomy. However, there were no consistent factors that distinguished which cases with elevated IOP at 1 day ultimately needed further therapy, nor did the 1-day postoperative examination predict which patients would have IOP elevation at 1 month. CONCLUSION: IOP 1 day after ALT is rarely elevated and does not correlate with IOP elevation at 1 month. Therefore, an IOP check at 1 day is not felt to be necessary for most patients.     

Intravascular ultrasound findings in stenting of unprotected left main coronary artery stenosis

We evaluated the role of intravascular ultrasound (IVUS) in 16 patients with unprotected left main coronary artery (LMCA) stenting compared with 80 patients with other (non-LMCA) native coronary artery stenting and found that (1) additional high-pressure or larger size balloon dilations were more frequently performed in LMCA stenting than in non-LMCA stenting (p <0.05) and (2) after IVUS-guided stent implantation, minimum lumen area was > or = 9 mm2 in 88% of patients who underwent LMCA stenting and in 19% of those who underwent non-LMCA stenting (p <0.001). IVUS guidance may be a more important adjunctive imaging modality in the stenting of unprotected LMCA stenoses than in stenting of non-LMCA stenoses.     

Somatostatin receptor desensitization in NG108-15 cells. A consequence of receptor sequestration

In NG108-15 cells inhibition of both N-type calcium channel current and adenylyl cyclase by somatostatin (SRIF) was not sustained but rapidly desensitized in the continued presence of the drug. The degree and rate of desensitization were concentration-dependent, and the desensitization was homologous with respect to the delta-opioid receptor. We have been unable to obtain evidence for the involvement of G protein-coupled receptor kinases (GRKs) in this desensitization. SRIF-induced desensitization of N-type calcium channel currents was not reduced in cells stably overexpressing a dominant negative mutant of GRK2 or following intracellular dialysis with GRK2- and GRK3-blocking peptides or with heparin. Inhibitors of protein kinase A, protein kinase C, and protein kinase G were also without effect. In contrast, both the rate and degree of SRIF-induced desensitization were reduced by pretreatment with phenylarsine oxide or concanavalin A, both inhibitors of receptor endocytosis. Furthermore, SRIF-induced desensitization was enhanced by monensin, which prevents receptor recycling back to the plasma membrane. Similarly, SRIF-induced desensitization of adenylyl cyclase inhibition was not reduced in cells stably overexpressing dominant negative mutant GRK2 but was reduced in cells pretreated with the receptor endocytosis inhibitor hyperosmotic sucrose or concanavalin A. These data are consistent with the view that SRIF-induced desensitization in NG108-15 cells results from receptor internalization.     

Laparoscopic splenectomy: outcome and efficacy in 103 consecutive patients

OBJECTIVE: To study the safety and efficacy of laparoscopic splenectomy (LS) in patients with predominantly benign hematologic disorders. SUMMARY BACKGROUND DATA: The technical feasibility of LS has been recently established. However, data regarding the efficacy of the procedure in a large cohort of patients are scarce. METHODS: One hundred three consecutive patients underwent LS between June 1992 and October 1997. Data were collected prospectively on all patients. RESULTS: Indications were idiopathic thrombocytopenic purpura (ITP), hereditary spherocytosis, autoimmune hemolytic anemia, thrombotic thrombocytopenic purpura, and others. Mean spleen size was 14 cm and mean weight was 263 g. Accessory spleens were found in 12 patients with ITP and in 5 patients without ITP. There were no deaths. Complications occurred in six patients, one requiring a second procedure for small bowel obstruction. Six patients received transfusions, and four procedures were converted to open splenectomy for bleeding. Mean surgical time was 161 minutes and was greater in the first 10 cases than the last 10. Mean postsurgical stay was 2.5 days. Thrombocytopenia resolved after surgery in 84% of patients with ITP, and hematocrit levels increased significantly in 70% of patients with chronic hemolytic anemias. A positive response was noted in 92% of patients with hereditary spherocytosis, without relapse for the duration of the observation. ITP relapsed in four patients during follow-up, three within 12 months. CONCLUSIONS: LS can be performed safely and effectively in a teaching institution. Rigorous technique will minimize capsular fractures, reducing the risk of splenosis. Accessory spleens can be successfully localized, thus improving response and limiting recurrence of ITP. LS should become the technique of choice for treatment of intractable benign hematologic disease.     

Dopamine receptor subtypes expressed in vertebrate (carp and eel) retinae: cloning, sequencing and comparison of five D1-like and three D2-like receptors

Eight dopamine receptor-like cDNA clones were isolated from the carp (Cyprinus carpio) retina and four dopamine receptor-like cDNA clones were isolated from the European eel (Anguilla anguilla) retina. These cDNA clones show high sequence and structural homology to the known dopamine receptor subtypes. The sequence similarity and phylogenetic analysis revealed that five subtypes (D1A3, D1A4, D1B, D1C and D1X) in the carp retina and four subtypes (D1A1, D1A2, D1B and D1C) in the eel retina are D1-like receptor subtypes, and three (D2, D4A and D4B) in the carp retina are D2-like receptor subtypes; no D2-like receptor was found in the eel. Carp D1A3 and D1A4, carp D4A and D4B, and eel D1A1 and D1A2 are highly homologous pairs of receptors which show significant, domain-specific differences to each other and to their species homologues. The structure of the third cytoplasmic loop in the carp D1X receptor was particularly different from the other D1-like receptors. The implications of these structural differences in terms of dopamine receptor activation and signalling are discussed. It is suggested that the known diverse physiological and pharmacological effects of dopamine on the retinal neurones are likely to be mediated through these multiple receptor subtypes which may be coupled to different signal transduction pathways.