Sympathetic skin response and R–R interval variation in chronic uremic patients

Sympathetic skin response (SSR) and R–R interval variation (RRIV) were studied in 36 chronic, nondiabetic uremics to compare with their nerve conduction studies (NCS) and clinical dysautonomia. Abnormal SSR was noted in 5 (13.9%) patients, abnormal RRIV in 14 (38.9%), and abnormal NCS in 26 (72.2%). The patients were classified into three groups: group (GP) 1: “normal,” n = 21 (58.3%), normal RRIV and SSR; GP 2: “isolated parasympathetic dysfunction,” n = 10 (27.8%), abnormal RRIV and normal SSR; and GP 3: “sympathetic sudomotor dysfunction,” n = 5 (13.9%), abnormal SSR. A significant difference in age was found among the three groups (GP 3 > GP 2 > GP 1; P < 0.0001, ANOVA). After controlling the age factor, we still noted a tendency toward increasing NCS disturbances (distal latency and nerve conduction velocity of peroneal nerve; P < 0.05, multiple regression analysis) and frequencies of clinical autonomic symptoms (postural dizziness and impotence; P < 0.05, Mantel–Hanszel test) from GP 1 to GP 3. Patients with abnormal SSR (GP 3) displayed significantly higher frequencies of postural dizziness and impotence, indicating the relationship between an absence of SSR and clinical dysautonomia. © 1994 John Wiley & Sons, Inc.     

Children hospitalized with influenza B infection

An outbreak of influenza virus type B infection occurred in Philadelphia from December, 1985, to April, 1986. During this epidemic 24 patients were admitted to Children's Hospital from whom influenza B was isolated from routine respiratory viral cultures. All were younger than 3 years of age. Clinical findings included fever (greater than or equal to 38 degrees C) (88%), rhinorrhea (62.6%), cough (50%), otitis (50%), rhonchi (42%), vomiting (38%), diarrhea (33%), rales (21%), pharyngitis (13%) and croup (4%). Remarkably 75% of the patients had underlying diseases which may have contributed to the severity of the infection. Nine (41%) patients had pneumonia. Two patients died of respiratory failure caused by overwhelming influenza B virus infection. Patients admitted to the hospital with respiratory and underlying diseases should have viral respiratory cultures which include influenza B.     

To die or not to die for neurons in ischemia,traumatic brain injury and epilepsy: a review on the stress-activated signaling pathways and apoptotic pathways

After a severe episode of ischemia, traumatic brain injury (TBI) or epilepsy, it is typical to find necrotic cell death within the injury core. In addition, a substantial number of neurons in regions surrounding the injury core have been observed to die via the programmed cell death (PCD) pathways due to secondary effects derived from the various types of insults. Apart from the cell loss in the injury core, cell death in regions surrounding the injury core may also contribute to significant losses in neurological functions. In fact, it is the injured neurons in these regions around the injury core that treatments are targeting to preserve. In this review, we present our cumulated understanding of stress-activated signaling pathways and apoptotic pathways in the research areas of ischemic injury, TBI and epilepsy and that gathered from concerted research efforts in oncology and other diseases. However, it is obvious that our understanding of these pathways in the context of acute brain injury is at its infancy stage and merits further investigation. Hopefully, this added research effort will provide a more detailed knowledge from which better therapeutic strategies can be developed to treat these acute brain injuries.     

Human mini-chromosomes in mouse embryonal stem cells

We have introduced human mini-chromosomes of 4 Mb and approximately 15 Mb in size into mouse embryonal stem cells. Although these human mini- chromosomes are stable in hamster and chicken cells, they re-arrange or segregate aberrantly in the embryonal stem cells and are rapidly lost in the absence of selection. However, one of the mini-chromosomes re- arranged, acquired mouse centromeric sequences and was then stably maintained for at least 60 population doublings in culture. This mini- chromosome, which is 4 Mb in size, is a candidate for a mouse germ line chromosome vector.      

Lack of STK11 gene expression in homozygous twins with Peutz-Jeghers syndrome

Clinical features of Peutz-Jeghers syndrome (PJS), an autosomal dominant disorder, include clusters of melanotic spots on the lips and limbs, polyposis of the gastrointestinal (GI) tract, and propensity to develop neoplasms of the GI tract, ovaries, testes, and other sites. We report twin sisters with PJS who were found to be homozygous, based on analyses of 9 DNA markers containing short tandem repeats (STR). Aberrant expression of a putative tumor suppressor gene, STK11, which encodes a serine threonine kinase, has been suggested as the etiologic factor in PJS. In both of the twin sisters with PJS, mRNA analyses by RT-PCR demonstrated a complete lack of STK11 gene expression. These results provide direct evidence that STK11 gene expression is abnormal in PJS. Detecting abnormal expression of the STK11 gene may serve as a molecular approach to the diagnosis of PJS and may facilitate genotype-phenotype correlations in PJS patients.