PubMed Health⌕ Search

Biomedical subjects

J J Lu

Publications and source records attributed to J J Lu.

At least 37 records · Page 2Linked to original sources

Ovarian epithelial tumor growth promotion by follicle-stimulating hormone and inhibition of the effect by luteinizing hormone.

OBJECTIVES: The role of gonadotropins in ovarian epithelial cancer development is still controversial. Follicle-stimulating hormone receptor (FSHR) status in ovarian epithelial tumors (OETs) and their presumed precursor lesions has never been studied in detail. The objective of this study was to examine whether FSHR is expressed in OETs and to investigate the possible different roles of the gonadotropins in ovarian cancer development. METHODS: Twenty ovarian epithelial inclusions (entrapments or invaginations of ovarian surface epithelium) from benign ovaries and 60 OETs including 12 cystadenomas, 18 borderline tumors, and 30 carcinomas were examined for FSHR expression by using reverse transcription polymerase chain reaction (RT-PCR), in situ hybridization (ISH), and immunohistochemistry (IHC). We also studied the mitogenic activity of FSH on two FSH and luteinizing hormone (LH) receptor-positive ovarian epithelial carcinoma cell lines (AO and 3AO) and on the modifying effect of LH on this activity. Growth-stimulating effects of the gonadotropins were tested in vitro with measurement of cell numbers, S-phase by flow cytometry, and changes in the cellular proliferative marker Ki-67. RESULTS: Positive FSHR mRNA expression by RT-PCR (the most sensitive method) was found in 100% of epithelial inclusions, 100% of cystadenomas, 94% of borderline tumors, and 60% of carcinomas. There was a nonstatistically significant trend of decreasing positivity with increasing carcinoma grade. ISH and IHC gave similar, but somewhat less sensitive, results. A dose-response effect was seen with FSH, with a 1.6-fold increase in cell numbers with a maximally stimulating FSH concentration of 40 IU/L for a period of 48 h. These proliferative cellular effects were not observed when the cells were stimulated by LH in the range 1 to 100 IU/L. Most significantly, the growth stimulating effects of FSH could be blocked by the simultaneous administration of LH. CONCLUSIONS: FSHR is present in the majority of ovarian epithelial inclusions and OETs. The steady decline of FSHR expression from benign cystadenoma to borderline tumor to carcinoma suggests that FSH may be needed in early ovarian cancer development. Gonadotropins, FSH and LH, may have different roles in ovarian cancer cell proliferation. FSH, not LH, may be an important ovarian epithelial cell growth-promoting factor. The "opposing" effect of LH on FSH stimulation may explain why high FSH levels at postmenopausal ages are not associated with great increases in ovarian cancer risk.

Adult↗

Reduction of BRCA1 expression in sporadic ovarian cancer.

OBJECTIVE: The purpose of this study was to examine BRCA1 expression and its relationship to cell proliferation in sporadic ovarian epithelial tumors (OETs). METHODS: We investigated BRCA1 expression and cell proliferative activity in 72 unselected OETs. They comprised 16 benign cystadenomas, 18 borderline (low malignant potential) tumors, and 38 carcinomas (OECs). These patients had no known family history of breast and/or ovarian cancer. BRCA1 and the cell proliferation marker, MIB-1, expressions in fixed tissue were investigated in all 72 cases by immunohistochemistry (IHC). BRCA1 mRNA in fresh frozen tissue samples from 20 of these cases was measured by a semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) method. RESULTS: The average percentage of BRCA1-positive cells was 5.6% in cystadenomas, 29.7% in borderline tumors, and 6.6% in OECs. The average decreased steadily with increasing grade of OECs: grade 1 (21.4%), grade 2 (1.1%), and grade 3 (0%). The average percentage of MIB-1-positive cells increased steadily from cystadenomas (7.5%) to borderline tumors (22.6%) to carcinomas (41.2%). BRCA1 expression was highly correlated with MIB-1 expression in cystadenomas and borderline tumors. Six of seven OECs negative for BRCA1 by IHC showed low levels of BRCA1 mRNA by RT-PCR. CONCLUSIONS: BRCA1 expression paralleled cell proliferation in benign and borderline OETs, but not in OECs. Sporadic OECs showed significantly reduced levels, rather than complete loss, of BRCA1 expression. The reduction was closely related to tumor grade. Reduction of BRCA1 expression may be of etiologic significance in the occurrence and progression of sporadic ovarian cancer.

Antigens, Nuclear↗

Decreased luteinizing hormone receptor mRNA expression in human ovarian epithelial cancer.

OBJECTIVES: The objective of this study was to examine the distribution and cellular localization of luteinizing hormone receptor (LHR) in ovarian epithelial tumors (OETs) and their presumed precursor lesions-ovarian epithelial inclusions (OEIs). The clinicopathologic correlation of the receptor expression in OET was also examined. METHODS: Fifteen microdissected samples of ovarian surface epithelium (OSE), 20 OEIs from benign ovaries, and 141 OETs, including 48 cystadenomas, 33 borderline tumors, 60 carcinomas, and 5 metastatic cancers, were examined for LHR expression by using reverse transcription polymerase chain reaction and in situ hybridization. LHR expression in tumor epithelium and tumor stroma was analyzed separately. The clinicopathologic correlation data were analyzed by standard analysis of variance and contingency table methods. RESULTS: LHR expression was identified in the majority of OSE and OEI samples. In OETs, LHR positivity was found in the epithelial cells in 27% of cases and in the stromal compartment in 37% of cases. LHR-positive stromal cells were mainly luteinized cells. Within the tumor epithelium, LHR expression was detected in 42% of benign, 24% of borderline, and 17% of malignant OETs. LHR expression in tumor stroma showed a similar trend of reduction from benign to malignant OETs. Within the 17 carcinomas, LHR was expressed in the epithelium in 47% of grade 1, 12% of grade 2, and only 5% of grade 3 cancers. The mean age of the LHR-positive group was younger than that of the receptor-negative patients. Compared with mucinous and other types of OETs, serous OETs showed higher LHR expression in the epithelium. Compared with the OETs removed in the different menstrual phases, OETs in the secretory phase showed higher LHR in the tumor stroma than in the proliferative phase. No receptor mRNA was detected in the epithelium of five carcinomas metastatic to the ovary. LHR transcription splicing variants from a single previous report were confirmed in this study. CONCLUSIONS: Malignant OETs have significant reduction of LHR expression compared with precursor lesions and benign and borderline OETs. LHR expression shows a steady decline from low-grade to high-grade ovarian cancer. The presence of LHR receptor in tumor epithelium suggests that luteinizing hormone in serum may have direct influence on tumor growth, whereas the receptor in tumor stroma may be indicative of a paracrine function of LH in the development of OETs.

Adolescent↗

Apoptosis may be an early event of progestin therapy for endometrial hyperplasia.

OBJECTIVE: The aim of this study was to investigate the role of apoptosis during progestin therapy for the treatment of endometrial hyperplasia. METHODS: Pre- and posttreatment paraffin-embedded endometrial tissue samples from 19 women with endometrial hyperplasia were examined for changes in glandular cellularity and apoptotic activity related to the administration of progestins. Twelve patients were successfully treated with progestin therapy and 7 patients failed treatment. Glandular cellularity was assessed based on calculating the average number of cells per gland obtained on histologic examination of hematoxylin and eosin stained tissue sections. Apoptotic activity was assessed on the same tissue sections by counting the average number of apoptotic cells per 10 high power fields (hpf) using the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling (TUNEL) assay. The effects of progesterone on apoptotic activity in a low-grade endometrial adenocarcinoma cell line (Ishikawa cells) was also examined using an ELISA cell death detection kit. RESULTS: Glandular cellularity significantly decreased with progestin therapy in both treatment outcome groups. The reduction in cells per gland was significantly greater in the group of successfully treated cases compared to the treatment failures (P = 0.005). However, within the successfully treated group, in situ detection of apoptotic cells using the TUNEL assay showed no statistical difference between pre- and posttreatment endometrial samples. Interestingly, a significant decrease in apoptosis was found in posttreatment samples of the group with persistent hyperplasia. The average number of apoptotic cells detected in 10 hpf was reduced from 7.9 prior to treatment to 3.1 after progestin therapy (P = 0.03). In the progesterone-treated Ishikawa cell line, an increase in apoptotic activity started at 24 h, reached a peak at 48 h, and continued up to 72 h of hormone treatment. At 48 h, apoptotic activity was 42.6% greater than in the untreated control (P = 0.04). By 72 h of progesterone treatment, apoptosis was 37.2% greater in the treated cells compared to the noninoculated cells (P = 0.04). CONCLUSIONS: Progestin-induced apoptosis may occur during the early period of treatment for endometrial hyperplasia. Compared to the fully responsive group, persistent endometrial hyperplasia may have intrinsically different molecular mechanisms in response to progestin therapy.

Adult↗

Tumor stroma as the main source of inhibin production in ovarian epithelial tumors.

PROBLEM: Elevated serum inhibin levels have been found in ovarian cancer patients; however, the source of the elevated inhibin is uncertain. Previous studies of activin in human ovarian cancer suggest that activin may promote the growth of the tumor. The aims of this study were to examine the source of elevated inhibin from ovarian epithelial tumors (OETs) and to preliminarily investigate the role of the gonadotropin-inhibin/activin relationship in the development of OET. METHOD OF STUDY: The protein and mRNA expression of alpha and betaA subunits of inhibin/activin were examined by immunohistochemistry (IHC) and reverse transcription polymerase chain reaction (RT-PCR) in 120 OETs, including 30 benign cystadenomas, 30 borderline tumors, and 60 carcinomas. Stromal and epithelial cells were microdissected from 23 OETs to further examine the expression of alpha and betaA subunits by RT-PCR. Dimeric inhibin A and activin A production were measured by using the two-site ELISA from three OET cell lines in culture under treatment of follicle-stimulating hormone (FSH) and luteinizing hormone (LH). RESULTS: betaA subunit was expressed in the epithelial component of 100% of the cystadenomas, in 80% of borderline tumors, and in 75% of the carcinomas, but not in tumor stroma. Inhibin alpha expression was not found in the epithelium of all OETs studied, but focal inhibin alpha immunoreactivity was seen in the tumor stroma (mainly luteinized stromal cells) in the majority of cases. Dimeric activin A was produced by all of the three OET cell lines with a 1.5-1.9-fold increment after FSH stimulation. However, activin A production was not augmented by LH treatment. No inhibin A was produced by the three OET cell lines with or without gonadotropin stimulation. CONCLUSIONS: The stroma of OET is the major source in the production of inhibin alpha (monomer). Dimeric inhibin A production may be the result of combined efforts of the tumor stroma (alpha subunit) and epithelium (betaA subunit). Cellular, compartmental expression of inhibin and activin subunits may play a role in the development of OET, although the mechanism remains undefined. The unopposed activin A production stimulated by FSH in OET cell lines suggests that activin production may represent one of the cellular mechanisms of growth promotion by FSH.

Activins↗

Quinupristin-dalfopristin resistance among gram-positive bacteria in Taiwan.

To understand quinupristin-dalfopristin resistance among clinical isolates of gram-positive bacteria in Taiwan, where this agent is not yet available for clinical use, we evaluated 1,287 nonduplicate isolates recovered from January 1996 to December 1999 for in vitro susceptibility to quinupristin-dalfopristin and other newer antimicrobial agents. All methicillin-susceptible Staphylococcus aureus (MSSA) isolates were susceptible to quinupristin-dalfopristin. High rates of nonsusceptibility to quinupristin-dalfopristin (MICs, >/=2 microg/ml) were demonstrated for the following organisms: methicillin-resistant S. aureus (MRSA) (31%), coagulase-negative staphylococci (CoNS) (16%), Streptococcus pneumoniae (8%), viridans group streptococci (51%), vancomycin-susceptible enterococci (85%), vancomycin-resistant Enterococcus faecalis (100%), vancomycin-resistant Enterococcus faecium (66%), Leuconostoc spp. (100%), Lactobacillus spp. (50%), and Pediococcus spp. (87%). All isolates of MSSA, MRSA, S. pneumoniae, and viridans group streptococci were susceptible to vancomycin and teicoplanin. The rates of nonsusceptibility to vancomycin and teicoplanin were 5 and 7%, respectively, for CoNS, ranging from 12 and 18% for S. simulans to 0 and 0% for S. cohnii and S. auricularis. Moxifloxacin and trovafloxacin had good activities against these isolates except for ciprofloxacin-resistant vancomycin-resistant enterococci and methicillin-resistant staphylococci. In Taiwan, virginiamycin has been used in animal husbandry for more than 20 years, which may contribute to the high rates of quinupristin-dalfopristin resistance.

Acetamides↗

Use of PCR with universal primers and restriction endonuclease digestions for detection and identification of common bacterial pathogens in cerebrospinal fluid.

We have designed a universal PCR capable of amplifying a portion of the 16S rRNA gene of eubacteria, including Staphylococcus aureus, Staphylococcus epidermidis, Streptococcus pyogenes, Streptococcus agalactiae, Streptococcus pneumoniae, Enterococcus faecium, Enterococcus faecalis, Mycobacterium tuberculosis, Legionella pneumophila, Escherichia coli, Klebsiella pneumoniae, Serratia marcescens, Enterobacter cloacae, Pseudomonas aeruginosa, Acinetobacter baumannii, Proteus mirabilis, Haemophilus influenzae, and Neisseria meningitidis. The sizes of the amplified products from various bacteria were the same (996 bp), but the restriction patterns of most PCR products generated by HaeIII digestion were different. PCR products from S. aureus and S. epidermidis could not be digested by HaeIII but yielded different patterns when they were digested with MnlI. PCR products from S. pneumoniae, E. faecium, and E. faecalis yielded the same HaeIII digestion pattern but could be differentiated by AluI digestion. PCR products from E. coli, K. pneumoniae, S. marcescens, and E. cloacae also had the same HaeIII digestion pattern but had different patterns when digested with DdeI or BstBI. This universal PCR could detect as few as 10 E. coli or 250 S. aureus organisms. Compared with culture, the sensitivity of this universal PCR for detection and identification of bacteria directly from 150 cerebrospinal fluids was 92.3%. These results suggest that this universal PCR coupled with restriction enzyme analysis can be used to detect and identify bacterial pathogens in clinical specimens.

Aged↗

Characterization of the first clinical isolate of vancomycin-resistant Enterococcus faecalis, AH803, in Taiwan.

We previously isolated a vancomycin-resistant strain of Enterococcus faecalis, designated AH803, from the sputum of a patient with pneumonia and bacteremia in Taiwan. AH803 was resistant to vancomycin (minimal inhibitory concentration, MIC = 512 micrograms/mL) but susceptible to teicoplanin (MIC = 8 micrograms/mL), and harbored the vanA gene but not the vanB gene. In this study, we further characterized E. faecalis AH803 and the plasmid it was found to contain. DNA from AH803 was analyzed for the presence of vanA and vanB resistance genes by polymerase chain reaction. The vancomycin resistant phenotype was transferable from AH803 to E. faecalis JH2-2, at a frequency of 4.8 x 10(-2). AH803 was also resistant to gentamicin and chloramphenicol, and these antibiotic resistance phenotypes cotransferred with vancomycin resistance. The genes responsible for resistance to all three antibiotics were located on a 42-kb conjugative plasmid (pBL101). This plasmid had the same restriction enzyme digestion patterns as Tn1546, found in pIP816 of E. faecalis BM4147. Epidemiologic studies of glycopeptide resistance should perhaps combine phenotypic and genotypic methods, rather than using phenotypic methods alone.

Bacterial Proteins↗

Characterization of a highly glycopeptide-resistant Enterococcus gallinarum isolate.

BACKGROUND AND PURPOSE: Adequate treatment of emergency infection involving antibiotic-resistant bacteria such as vancomycin-resistant Enterococcus requires a convergence of clinical and bacteriologic techniques. An isolate of Enterococcus gallinarum, designated as TSGH63, is known to be uncommonly vancomycin-resistant. This study investigated the genetic determinant for this unique characteristic. METHODS: After completing the conventional identification and sensitivity tests, the genomic content of E. gallinarum TSGH63 was extracted and analyzed by pulse-field electrophoresis. A set of specific primers for vanA, vanB, vanC1, and vanC2/C3 genes was then applied in a multiplex polymerase chain reaction (PCR) to differentiate its genetic content. To locate the determinant for high vancomycin resistance, the electrophoresis profile was further analyzed by Southern blot using the digoxigenin (DIG)-labeled vanA gene probe. Finally, interspecies transfer of the vancomycin-resistance determinant of E. gallinarum TSGH63 was tested by a conjugation experiment in vitro. RESULTS: A 50-kb plasmid was identified in the analysis of the genomic extract of E. gallinarum TSGH63 by pulse field electrophoresis. Using multiplex PCR, we demonstrated that E. gallinarum TSGH63 harbors a vanA gene in addition to a vanC1 gene. The DIG-labeled vanA gene-specific probe bound to the plasmid exclusively on the Southern blot. The plasmid-carried vanA gene, but not the vanC1 gene, was found to be transferable from TSGH63 to E. faecalis JH2-2 by conjugation in vitro. CONCLUSIONS: This is the first report of isolation of E. gallinarum with a high level of resistance to glycopeptides in Taiwan. The demonstrated interspecies transfer of the vancomycin-resistance gene highlights the importance of stringent control of the use of vancomycin.

Conjugation, Genetic↗

Detection of circulating cancer cells by reverse transcription-polymerase chain reaction for uroplakin II in peripheral blood of patients with urothelial cancer.

Few attempts have been made at the molecular detection of urothelial cancer cells in the blood or lymph nodes mainly because of an absence of good candidate molecular or genetic changes specific to urothelial cancer or urothelium. In 1990, however, genes that encode urothelium-specific transmembrane proteins, uroplakins (UPs), were cloned. We have established a method of detecting circulating cancer cells in peripheral blood of patients with transitional cell carcinoma by nested reverse transcription-PCR assay for UP II. UP II mRNA-positive cells were detected in 3 (10.3%) of 29 patients with superficial cancers (pTa-1N0M0), 4 (28.6%) of 14 patients with muscularly invasive cancers (pT2-4N0M0), 2 (40.0%) of 5 loco-regional node-positive patients (pN1-2M0), and 6 (75.0%) of 8 patients with distant metastases. Positive rates, therefore, increased with tumor extension (P = 0.0033, Kruskal-Wallis test). Furthermore, sequential blood sampling was performed in three patients with metastases during and after systemic chemotherapy, and UP-II-positive cells were found to have disappeared in two patients who responded well to the systemic chemotherapy. These results suggest that our nested reverse transcription-PCR assay for UP II is highly specific and might be used as a tumor marker for molecular staging of urothelial cancers, although the sensitivity is not so optimal.

Adult↗

Tuberculosis of skeletal muscle in a case of polymyositis.

We describe a patient with polymyositis receiving corticosteroid therapy, who presented with persistent fever and mass lesion at the left thigh. Surgical exploration and mycobacterial culture proved to be Mycobacterium Tuberculosis infection involving the semitendinous muscle of the left thigh. Suitable surgical debridement, anti-TB medications, and sufficient corticosteroid administration resulted in a good control of both polymyositis and the tuberculous infection.

Female↗

Antimicrobial susceptibilities of clinical isolates of vancomycin-resistant enterococci in Taiwan.

To understand the antimicrobial resistance patterns of vancomycin-resistant enterococci in Taiwan, we tested the in vitro activities of 10 antimicrobial agents against 71 clinical isolates (39 of Enterococcus faecalis and 32 of Enterococcus faecium) by means of the agar dilution method. Resistance was determined on the basis of the minimum inhibitory concentration (MIC) of each antimicrobial agent--MIC50 and MIC90 (minimum concentrations required to inhibit growth of 50% and 90% of isolates, respectively) were determined. No beta-lactamase producers were identified with the cefinase test. All E. faecalis isolates were susceptible to penicillin and ampicillin, and 97% of these isolates were resistant to teicoplanin (vanA phenotype). Of the E. faecium isolates, 75% were susceptible to teicoplanin (vanB phenotype) and most were resistant to penicillin (94%) and ampicillin (94%). Quinupristin/dalfopristin was markedly less active against E. faecalis than E. faecium isolates (MIC50, 64 vs 2 micrograms/mL; MIC90, 128 vs 8 micrograms/mL; susceptibility rates, 3% vs 81%). Five of the eight vanA phenotype E. faecium isolates and one of the 24 vanB phenotype E. faecium isolates were resistant to quinupristin/dalfopristin. The activity of rifampin was also species-specific, with E. faecium being markedly less susceptible to this agent than E. faecalis (MIC50, 16 vs 1 microgram/mL; MIC90, 64 vs 4 micrograms/mL). Our data suggest the potential of teicoplanin and quinupristin/dalfopristin as appropriate antimicrobial agents in the treatment of infections caused by vanB phenotype E. faecium. Penicillin, ampicillin, and rifampin alone, or preferably in combination with other agents, appear to be the most appropriate agents for the treatment of vancomycin-resistant E. faecalis infections in Taiwan.

Drug Resistance, Microbial↗

Varicella arthritis diagnosed by polymerase chain reaction.

We report a 2-year-old girl who developed acute arthritis of the left knee 4 days after the onset of a typical varicella infection. She was first thought to have pyogenic arthritis caused by Staphylococcus aureus. Accordingly, oxacillin was administered upon hospitalization. On the third day after hospitalization, bacterial cultures of the synovial fluid and blood showed no growth and oxacillin was discontinued. Although a viral culture of the synovial fluid for varicella-zoster virus (VZV) was negative, varicella DNA was identified by means of polymerase chain reaction (PCR) with VZV-specific primers. The patient recovered spontaneously. To differentiate this condition from septic arthritis is important. PCR is a sensitive technique that can demonstrate the presence of VZV DNA in synovial fluid, even if viral cultures are negative.

Arthritis, Infectious↗

Alcohol metabolism and cardiovascular response in an alcoholic patient homozygous for the ALDH2*2 variant gene allele.

BACKGROUND: Alcohol metabolism is one of the biological determinants that can influence drinking behavior. Alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) are the principal enzymes involved in ethanol metabolism. Allelic variation of the ADH and ALDH genes can significantly affect vulnerability for the development of alcoholism. Homozygosity of the variant ALDH2*2 allele previously was believed to fully protect East Asian populations against the development of alcoholism. METHODS: Eighty Han Chinese alcoholics who met DSM-III-R criteria for alcohol dependence and 144 nonalcohol-dependent subjects were recruited and their data combined with data from 340 alcohol-dependent and 545 nonalcohol-dependent subjects described in an earlier report (Chen et al., 1999) to assess risk for alcoholism by logistic regression analysis. Genotypes of ADH2, ADH3, and ALDH2 were determined by polymerase chain reaction and restriction fragment length polymorphism. The ALDH2 genotype was confirmed by direct nucleotide sequencing. Blood ethanol concentration was determined by headspace gas chromatography and acetaldehyde concentration by high-performance liquid chromatography with fluorescence detection of the derivatized product. Cardiovascular hemodynamic parameters were measured by two-dimensional Doppler echocardiography and sphygmomanometry. Extracranial arterial blood flow was measured by Doppler ultrasonography. RESULTS: An alcohol-dependent patient was identified to be ALDH2*2/*2, ADH2*2/*2, and ADH3*1/*2. Following challenge with a moderate oral dose of ethanol (0.5 g/kg of body weight), the patient exhibited peak concentrations for ethanol (55.7 mg/dl) and acetaldehyde (125 microM). During 130 min postingestion, the patient generally displayed similar or even less intense cardiovascular hemodynamic alterations when compared to a previously published study of nonalcoholic individuals with ALDH2*2/*2 who had received a lower dose of ethanol (0.2 g/kg). Logistic regression analysis of the combinatorial genotypes of ADH2 and ALDH2 in 420 alcohol-dependent and 689 nonalcohol-dependent subjects indicated that risk for alcoholism was 100-fold lower for the ADH2*2/*2-ALDH2*2/*2 individuals than the ADH2*1/*1-ALDH2*1/*1 individuals. CONCLUSIONS: The gene status of ALDH2*2/*2 alone can tremendously but not completely (as thought previously) protect against development of alcohol dependence. Individuals carrying the combinatorial genotype of ADH2*2/*2-ALDH2*2/*2 are at the least risk for the disease in East Asians. Physiological tolerance or innate insensitivity to the accumulation of blood acetaldehyde following alcohol ingestion may be crucial for the development of alcoholism in individuals homozygous for ALDH2*2.

Adolescent↗

Tuberculous meningitis in a Filipino maid.

Tuberculous meningitis, while not uncommon in Taiwan, has not been reported among foreign workers. We report the first case of tuberculous meningitis in a 37-year-old Filipino maid in Taiwan, who presented with headache, fever and vomiting. She had been well before this episode and the small screening films of the chest radiograph obtained on her arrival in Taiwan 15 months previously, and every 6 months thereafter showed no evidence of tuberculosis. The suspicion of tuberculous meningitis was delayed until disturbance of consciousness manifested and a standard chest radiograph showed a diffuse miliary pattern in both lung fields. A cerebrospinal fluid sample that was sent for a polymerase chain reaction-based assay specific for Mycobacterium tuberculosis showed a positive result. The patient recovered with sequelae of mildly incoherent speech and urinary incontinence after antituberculous medication and short-course steroid treatment. Clinicians should be aware of the possibility of tuberculous meningitis in foreign workers with complaints of fever and headache. Because high-quality chest radiographs are a prerequisite for early detection of pulmonary tuberculosis, we recommended that standard posterior-anterior chest radiographs should be obtained as part of the routine health examination for foreign workers.

Aged↗

Antimicrobial susceptibility of Clostridium difficile by E test.

The in vitro inhibitory activity of 11 antimicrobials against 44 clinical isolates of Clostridium difficile was investigated. Minimum inhibitory concentrations (MICs) were determined using E test. Metronidazole (MIC90 0.38 microg/mL), teicoplanin (MIC90 0.75 microg/mL) and vancomycin (MIC90 1.0 microg/mL) were very active against the isolates examined, whereas, resistance to imipenem, cefoxitin, clindamycin and ciprofloxacin was found in most of the tested strains. We concluded that teicoplanin warrants clinical trials to determine its adequate dosage to treat C. difficile infection. The commonly used regimens to treat intra-abdominal and/or anaerobic infections (eg. imipenem, cefoxitin, clindamycin or ciprofloxacin) need special attention, while considering the side effects of C. difficile-associated diarrhea.

Ampicillin↗

HPV-associated cervical cancers show frequent allelic loss at 3p14 but no apparent aberration of FHIT mRNA.

The genetic aberration involved in the loss of heterozygosity (LOH) at 3p14 has recently been attributed to the disruption of the FHIT gene in many cancers. This study analyzed HPV DNA and allelic status of 5 microsatellite markers spaning 3p13-3p25 in 57 cases of cervical cancer. With no homozygous deletion found in any case, a 39% overall frequency of LOH was noted. The presence of tumorigenic HPV DNA (91%) did not correlate with the allelic loss at any marker, including THRB (3p22-24) and D3S1228 (3p14) which were found with high LOH rates of 43% (12/28) and 37% (11/30), respectively. Further analysis of FHIT mRNA in 29 cancers by reverse transcription (RT)-PCR showed a full-length transcript in all cases. However, additional minor transcripts were occasionally observed in cancer tissues (9/29) as well as in normal tissues (12/31) by nested PCR of the RT products. Sequence analysis of these transcripts showed exclusive internal exon deletions, suggesting a source of minor splicing variants. No apparent mutation of the mRNA sequences was found in 8 transcripts examined, except for a silent polymorphism and a site of alternative splicing. The results suggest that, although frequently reported to be abrogated in several cancers, the mRNA of FHIT remains intact in cervical cancer. Other genes closely linked to FHIT may be responsible for frequent LOH at 3p14 observed in cervical cancer.

Acid Anhydride Hydrolases↗