Lionfish on the Loose in the Waters off St Vincent

Objective

The purpose of this study was to determine if the exotic venomous species, Pterois volitans (lionfish) had reached as far south as St Vincent in the Caribbean. This predatory marine fish has successfully invaded the waters of the Western Atlantic and the Caribbean. Such success as an exotic invasive species is rare for a predatory marine fish. It is possible that the fish are growing larger and spreading faster than anticipated, thanks to a lower burden of parasites and a paucity of natural predators in their new environment. But prior to this report, no sightings of this species this far south had been reported.

Methods

The authors conducted a search along with the help of local divers and fishermen in the waters of St Vincent.

Results

Approximately one year after the initiation of the search, a juvenile specimen was positively confirmed and captured off the southern coast of St Vincent.

Conclusions

The exotic predatory and venomous red lionfish, Pterois volitans, has successfully invaded marine waters as far south as the Windward Islands. Fishermen in these regions should be aware of this venomous species in the region and physicians must be aware of how to manage stings from such animals.     

脑复清胶囊中阿魏酸的含量测定研究

目的：建立薄层扫描法测定脑复清胶囊中阿魏酸含量的方法。方法：采用碱水提取,酸化后以醋酸乙酯萃取脑复清胶囊中阿魏酸,薄层法测定含量。结果：本方法线性方程为y=127997.95x 1090.60,r=0.9996(n=5),线性范围为0.50-2.53ug,同板精密度试验：RSD＝4．40％（n=5)异板精密度试验。RSD＝4．65％（n=5),平均加样回收率98．28％,结论：薄层扫描法可作为脑复清胶囊中阿魏酸的含量测定8方法,本实验研究为该产品的质量控制提供了可靠依据。     

Defects in neurofibromatosis 2 protein function can arise at multiple levels

Neurofibromatosis 2 (NF2) is an inherited cancer syndrome resulting from mutations in the NF2 tumor suppressor gene. Analysis of NF2 mutations has revealed some general genotype-phenotype correlations. Severe disease has been associated with mutations that produce a premature termination while more mild disease has been associated with missense mutations. Here, we provide experimental proof for these genotype-phenotype correlations by demonstrating that nonsense mutations fail to produce stable merlin protein while missense mutations result in the generation of merlin proteins defective in negative growth regulation. This inability to suppress cell growth may result from defects in the function of merlin at several levels, including failure to form an intramolecular complex. Based on these findings, we propose a model for merlin growth suppression that provides a framework for analyzing NF2 patient mutations and merlin function.      

Detecting pre-ovulatory luteinizing hormone surges in urine

The study objectives were to determine (i) if pre-ovulatory luteinizing hormone (LH) surges, undetected in urine by two immunoradiometric assays (IRMA), were detectable by an ultrasensitive immunofluorometric assay (IFMA) and (ii) the influence of creatinine adjustment on the detection and timing of the urinary LH surges. Daily urine specimens were contributed by healthy 25-36 year old volunteers during 14 ovulatory menstrual cycles for an epidemiological study conducted in 1983-1985. Specimens were selected as having been previously assayed by two IRMA without consistently detecting LH surges. These urine specimens were remeasured using an IFMA and adjusted for creatinine concentration. IFMA measurements revealed unambiguous LH surges in all cycles. Adjusting IRMA urinary LH values for creatinine concentrations revealed previously undetected LH surges in four of eight cycles. Creatinine adjustment also altered the timing of IRMA and IFMA LH surges by 1-5 days. These results demonstrate an IFMA that detects pre- ovulatory LH surges in unpreserved, frozen urine from cycles where such surges were previously undetectable. Further, creatinine adjustment can markedly affect detection and timing of the onset and peak of the urinary LH surge. While our analysis suggests that this adjustment improves the validity of the LH measure, this requires further investigation.