Birth weight, respiratory distress syndrome, and cognitive development. A four-year follow-up of preterm infants

This study examined the relationship of respiratory distress syndrome (RDS) and birth weight to cognitive development in 30 white, middle-class, low-birth-weight, preterm infants. Cognitive ability was assessed at 12, 36, and 48 months of age. No significant difference was found at any age between children who had and did not have RDS during the neonatal period. Children with birth weights of 1500 g or less were found to have lower scores than those with birth weights greater than 1500 g in the first year of life. However, the difference diminished with increasing age.     

Complications of general anesthesia using nitrous oxide in eyes with preexisting gas bubbles

PURPOSE: To present the visual and anatomical outcomes for patients with intraocular gas placed during vitreoretinal surgery who subsequently underwent surgery wherein general anesthesia with nitrous oxide was used. METHODS: The authors reviewed the charts of patients who had undergone vitreoretinal surgery where a long-acting gas tamponade had been used. These patients underwent additional surgery for a variety of reasons at five different institutions and had nitrous oxide used during general anesthesia. The authors reviewed the preoperative and postoperative findings for patients receiving nitrous oxide following vitreoretinal surgery with gas tamponade. RESULTS: The authors reviewed findings for five eyes of five patients. All eyes that underwent general anesthesia using nitrous oxide had significant preexisting intraocular gas bubbles ranging from 40% to 90%, and the surgical procedures lasted from 1 to 4 hours. These eyes were followed from 2 months to 9 years (median follow-up, 4 years). Four of five eyes had a final vision of 20/200 or worse and significant optic atrophy at the time of the last follow-up examination. Three eyes had no light perception. CONCLUSION: The use of nitrous oxide during general anesthesia in gas-filled eyes may have disastrous visual results caused by gas expansion and elevated intraocular pressure. Patients must be advised of the potentially catastrophic results of undergoing general anesthesia before their intraocular gas bubble has resorbed. The use of nitrous oxide for patients with intraocular gas should be avoided. It may be prudent for patients with intraocular gas to wear notification bracelets warning anesthesiologists about the presence of intraocular gas lest emergency surgery be needed by a patient unable to advise anesthesia personnel about the potential danger.     

Intrascleral implantation of glass beads during evisceration

BACKGROUND AND OBJECTIVE: To review the results after small glass bead implantation in the scleral cavity during evisceration. MATERIALS AND METHODS: In this retrospective study, we retrieved the follow-up data of 17 patients who underwent evisceration with glass bead implantation from 1993 to 1996. RESULTS: All patients achieved good cosmetic results with good motility of the prosthesis. Complications included transient chemosis at the early postoperative period in 3 patients (17.6%), 1 patient (5.9%) with local dehiscence of the wound, 1 patient developed a cyst in the socket (5.9%), and 1 patient was afflicted with thinning of the conjunctiva over the surgical wound. CONCLUSION: The use of glass beads to fill the scleral cavity during evisceration has the advantage of an excellent fit in accordance with the scleral cavity volume, as well as ease of treatment in case of extrusion. The prosthesis movement is good because of its engagement with the scleral bulges caused by the glass beads.     

Imexon activates an intrinsic apoptosis pathway in RPMI8226 myeloma cells

Imexon is a new antitumor agent with high activity in multiple myeloma. This drug induces apoptosis, oxidative stress and mitochondrial alterations. However, it was unknown whether imexon activates an intrinsic apoptotic pathway that is associated with activation of caspase-9 or an extrinsic pathway that is induced by receptor-mediated signals such as Fas ligand characterized by caspase-8 activation. In addition, we wanted to investigate the effect of imexon on Bcl-2 family proteins. In RPMI8226 myeloma cells, imexon activated caspase-9 and -3 in a time- and concentration-dependent manner. In contrast, cleavage of procaspase-8 was observed late and only after exposure to very high concentrations of imexon. Confocal microscopy confirmed that caspase-3 is also activated after treatment with imexon. High imexon concentrations activated caspase-3 and -9 at 12 h, while caspase-8 activation occurred only at 48 h. Imexon cytotoxicity was unchanged in three RPMI8226 cell lines with different levels (low, medium and high) of FAS expression. Similarly, the levels of Bcl-2, Bax and Bcl-xL were unchanged in imexon-treated cells. However, Bcl-xL was translocated to the mitochondria. These data suggest that imexon-induced oxidation activates the intrinsic or mitochondrial pathway of apoptosis, involving cytochrome release and activation of caspase-9 and -3.     

Lyme disease and the peripheral nervous system

Lyme disease, the multisystem infectious disease caused by the tick-borne spirochete Borrelia burgdorferi, causes a broad variety of peripheral nerve disorders, including single or multiple cranial neuropathies, painful radiculopathies, and diffuse polyneuropathies. Virtually all appear to be varying manifestations of a mononeuropathy multiplex. Diagnosis requires that the patient should have had possible exposure to the only known vectors, Ixodes ticks, and also have either other pathognomonic clinical manifestations or laboratory evidence of exposure. Treatment with antimicrobial regimens is highly effective. The mechanism underlying these neuropathies remains unclear, although interactions between anti-Borrelia antibodies and several peripheral nerve constituent molecules raise intriguing possibilities.     

A conceptual approach to the patient with metabolic acidosis. Application to a patient with diabetic ketoacidosis

We shall illustrate that management of patients with an acid-base disorder could be improved if the acid-base analysis was based on a better understanding of basic concepts of physiology. Three concepts of acid-base physiology and their clinical implications are emphasized in a patient with diabetic ketoacidosis. First, when an acid is produced from neutral precursors in the body, there is a net increase in the number of hydrogen ions (H(+)) and new anions. The corollary is that H(+) will be removed when the accompanying anion is metabolized to a neutral end-product or is excreted in the urine with H(+) or ammonium (NH(4)(+)). Second, buffering of H(+) is beneficial if H(+) are removed by bicarbonate rather than being able to bind to proteins. This latter function depends on having a low tissue PCO(2), due to a combination of hyperventilation plus an adequate blood flow rate to vital organs. Third, the kidneys add new bicarbonate to the body when NH(4)(+) is excreted with chloride ions.     

Focal segmental glomerular sclerosis in two patients with Addison's disease: any more than fortuitous development of glomerular disease?

Adjustment of the mineralocorticoid activity under substitution therapy is of primary importance in Addison's disease. We report the clinical and biological conditions of 2 patients with Addison's disease who developed nephrotic proteinuria during their deficient mineralocorticoid state. Renal biopsy was performed and the specimens processed using conventional histochemistry, Congo red staining, and indirect immunofluorescence. The renal biopsy specimens showed focal segmental glomerular sclerosis and nodular deposits of IgM and C3. Negative for Congo red staining. Serum complement, circulating immune complexes, and anti-DNA and hepatitis B and C and human immunodeficiency virus antibodies were all normal or negative. Absence of vesicoureteral reflux was assessed by X-ray studies. Our observations suggest that deficiency in mineralocorticoid substitution therapy inducing a status of hyperreninemia could play a role in the development of focal segmental glomerulosclerosis in patients with Addison's disease.     

Ethyl pyruvate prevents lethality in mice with established lethal sepsis and systemic inflammation

Sepsis, a potentially fatal clinical syndrome, is mediated by an early (e.g., tumor necrosis factor and IL-1) and late [e.g., high mobility group B-1 (HMGB1)] proinflammatory cytokine response to infection. Specifically targeting early mediators has not been effective clinically, in part because peak mediator activity often has passed before therapy can be initiated. Late-acting downstream effectors, such as HMGB1, that mediate sepsis lethality may be more relevant therapeutic targets. Ethyl pyruvate (EP) recently was identified as an experimental therapeutic that significantly protects against lethal hemorrhagic shock. Here, we report that EP attenuates lethal systemic inflammation caused by either endotoxemia or sepsis even if treatment begins after the early tumor necrosis factor response. Treatment with EP initiated 24 h after cecal puncture significantly increased survival (vehicle survival = 30% vs. EP survival = 88%, P < 0.005). EP treatment significantly reduced circulating levels of HMGB1 in animals with established endotoxemia or sepsis. In macrophage cultures, EP specifically inhibited activation of p38 mitogen-activated protein kinase and NF-kappaB, two signaling pathways that are critical for cytokine release. This report describes a new strategy to pharmacologically inhibit HMGB1 release with a small molecule that is effective at clinically achievable concentrations. EP now warrants further evaluation as an experimental "rescue" therapeutic for sepsis and other potentially fatal systemic inflammatory disorders.     

Lack of seasonal rhythms in central serotonergic function in boys with ADHD

This study examined seasonal variations in central 5-HT function in a relatively large sample of prepubertal boys with attention-deficit/hyperactivity disorder (ADHD). In addition, seasonal differences in central 5-HT function among aggressive and non-aggressive children in the sample were explored. Ninety-three boys with ADHD were divided into aggressive (n=54) and nonaggressive (n=39) groups based on parental responses to interviews and ratings of behavior. Central 5-HT function was assessed by measuring the prolactin response to a single 1 mg/kg oral dose of d,l-fenfluramine. The prolactin values were derived from different children over the course of eight years, but were collapsed across years and analyzed in terms of day of the year. Cosinor analysis revealed no annual, bi-annual, 3-monthly, 2-monthly, monthly, or bi-monthly rhythms in the prolactin response in the entire sample of boys with ADHD. Moreover, there was no evidence of seasonal differences in the prolactin response between the aggressive and non-aggressive subgroups. These results indicate that seasonality-related variance is not a threat to the validity of the neurochemical procedure and does not account for the inconsistencies in the studies of central 5-HT and aggression in children with ADHD.