Oral clonidine pretreatment for haemodynamic stability during craniotomy.

We have studied the effect of clonidine pretreatment on cardiovascular responses to various stimuli during craniotomy. Fifty-eight patients (ASA Class I-II), scheduled for supratentorial surgery, were randomly given either oral clonidine, mean dose 3.6 micrograms/kg (n = 28), or oral diazepam, 0.2 mg/kg (n = 30), ninety to one hundred minutes before surgery. Anaesthesia was induced with thiopentone and maintained with nitrous oxide:oxygen, pentazocine and halothane. Pancuronium was used as a neuromuscular blocker. Mean arterial pressure and heart rate were recorded before and after several stimuli. In the clonidine group hypertensive response was significantly less on laryngoscopy (6.5% increases versus 11.2% in the diazepam group), intubation (9.2% versus 16.5%), Mayfield clamp application (14.5% versus 29.91%) and after skin infiltration with lignocaine-adrenaline solution (2.95% versus 5.42%). Heart rate response to laryngoscopy, intubation and skin infiltration was also significantly attenuated in the clonidine group. The sleep dose of thiopentone was smaller in patients pretreated with clonidine. Patients in the diazepam group required more medical intervention. No adverse effect occurred in any patient.     

Inherited chondrodysplasia punctata due to a deletion of the terminal short arm of an X chromosome

We studied two families with an inherited deletion of the short arm of an X chromosome (Xp) in which affected male offspring have epiphyseal stippling in infancy (chondrodysplasia punctata), nasal hypoplasia, ichthyosis, and mental retardation. The presence of ichthyosis and the apparent pattern of X-linked recessive inheritance prompted investigation of the short arm of the X chromosome through studies of genetic markers and focused cytogenetic analysis. Biochemical studies suggested that there was a deletion of three genes previously mapped to the X-chromosome short arm, including the steroid sulfatase locus, the Xg locus, and the M1C2X locus. Prometaphase chromosomes demonstrated a deletion of Xp at p22.32 in the affected boys, in their obligate-carrier mothers, and in 11 of 25 women at risk as potential carriers. The women carrying the Xp deletion had normal gonadal function and fertility but were shorter than the noncarriers in their families (P less than 0.00001). These findings have implications for the genetic organization of this portion of the human X chromosome and demonstrate that small cytogenetic abnormalities may account for disorders with apparent mendelian patterns of inheritance.     

Listeria--review of epidemiology and pathogenesis.

Listeria monocytogenes (commonly called Listeria) is a Gram-positive facultatively intracellular foodborne pathogen often found in food and elsewhere in nature. It can cause a rare but serious disease called listeriosis, especially among pregnant women, the elderly or individuals with a weakened immune system. In serious cases, it can lead to brain infection and even death. Listeria is more likely to cause death than other bacteria that cause food poisoning. In fact, 20 to 30% of food borne listeriosis infections in high-risk individuals may be fatal. Recent technological developments have increased the ability of scientists to identify the cause of foodborne illnesses. L. monocytogenes has been used as a model organism for the study of intracellular parasitism. Whilst the basic mechanisms of cellular pathogenesis have been elucidated by a series of elegant studies, recent research has begun to focus upon the gastrointestinal phase of L. monocytogenes infection. Epidemiological studies of outbreaks of human disease now demonstrate that the pathogen can cause gastroenteritis in the absence of invasive disease and associated mortality. Elucidation of whole genome sequences and virulence determinants have greatly contributed to understanding of the organism and its infection pathways.     

Growth suppression of hybrids between transformed cells and normal fibroblasts in serum-free medium: Correlation with retention of human chromosomes

Somatic cell hybrids formed by crossing PG19 mouse melanoma cells with mouse embryo fibroblasts have a reduced ability to proliferate in growth factor-unsupplemented serum-free medium relative to the parental melanoma cells. The suppression of growth of the hybrid cells in serum-free medium is attributable to a strict requirement of these cells for polypeptide growth factors (insulin plus platelet-derived growth factor, fibroblast growth factor, or epidermal growth factor). In contrast, the parental melanoma cells are able to grow without exogenously added growth factors. Fifteen hybrids derived from crosses between mouse L cells and normal human skin fibroblasts also have been tested for ability to grow in growth factor-unsupplemented serum-free medium. Depending on which human chromosomes are retained, growth of these hybrids in serum-free medium is also suppressed relative to growth of the L cell parent. There appear to be several genes on different chromosomes that are involved in suppression of serum-free growth of the fibroblast × L cell hybrids. One weak suppressor gene appears to be on the human X chromosome.     

Assignment of human 3-hydroxy-3-methylglutaryl coenzyme A reductase gene to q13 → q23 region of chromosome 5

We have used hamster cDNA probes for 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase (HMGCR) to determine the chromosomal location of the human gene for HMG CoA reductase. Southern blot analysis of genomic DNA from 16 independent mouse-human somatic cell hybrids showed that the human gene for HMG CoA reductase resides on chromosome 5. Analysis of Chinese hamster-human somatic cell hybrids selectively retaining human 5 or a portion of it showed that the gene locus for HMG CoA reductase can be assigned to the q13 q23 region of chromosome 5.     

An evaluation of the inactive mouse X chromosome in somatic cell hybrids

The expression of mouseZfx, Rps4, Ube1x, andXist was evaluated in hamstermouse somatic cell hybrids containing either an active or an inactive mouse X chromosome using polymerase chain reaction of reverse transcribed RNA (RT-PCR). The results showed thatZfx, Rps4, andUbe1x are expressed exclusively from the active mouse X, whileXist is expressed exclusively from the inactive X. These findings confirm the pattern of X inactivation for these mouse genes reported previously based on expression in somatic tissues of F₁ females from interspecific crosses. These results demonstrate the existence of differences between human and mouse X inactivation, as the corresponding human genes,ZFX, RPS4X, andUBE1 escape X inactivation.