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B T Teh

Publications and source records attributed to B T Teh.

108 records · Page 6Linked to original sources
PubMed1996

Malposition of a long central venous catheter in the right inferior thyroid vein--a case report.

This case report hopes to bring to attention the possibility of malposition and ligation of a long central venous catheter in a central venous tributary in the course of major neck surgery. A 49-year-old gentleman underwent total laryngectomy and right radical neck dissection for laryngeal carcinoma. A long central venous catheter was inserted via the right basilic vein. This was subsequently found to have malpositioned into the right inferior thyroid vein and ligated. It required an exploration of the neck wound to remove the ligated catheter.

Catheterization, Central Venous↗
PubMed1995

Altered endogenous growth hormone secretory kinetics and diurnal GH-binding protein profiles in adults with chronic liver disease.

OBJECTIVE: Increased serum GH concentrations and GH responses to a variety of stimuli have been reported in patients with chronic liver disease (CLD). We investigated the pulsatile pattern of endogenous GH release and GH-binding protein (GHBP) and insulin-like growth factor-I (IGF-I) diurnal profiles in adults with cirrhosis, in comparison with healthy, matched control subjects. DESIGN: Case-control, cross-sectional. PATIENTS: Seven patients with biopsy proven cirrhosis, and sex, age, height, weight and oestrogen status matched controls. MEASUREMENTS: Serum immunoreactive GH concentrations in samples collected at 20-minute intervals for 24 hours were analysed using a multi-parameter deconvolution method to simultaneously resolve endogenous GH secretory and disappearance rates. Diurnal patterns of GHBP (specific immunoprecipitation method) and serum IGF-I (RIA after acid-ethanol extraction) were assessed. RESULTS: The mean daily GH secretion rate in patients with CLD was increased (210 +/- 93 vs 100 +/- 55 mU/I/day; P = 0.025), and GH disappearance half-time was prolonged (43 +/- 10 vs 24 +/- 9 min; P = 0.006) compared to controls. Detectable GH secretory bursts were more frequent in patients with CLD (10 +/- 1 vs 6 +/- 3/day; P = 0.038), but of similar mean mass (21 +/- 10 vs 17 +/- 8 mU/I) compared to controls. In patients with CLD, mean serum GHBP was slightly lower (63 +/- 36 vs 71 +/- 14% pooled control; P > 0.1). Fasting serum IGF-I concentrations (after size-exclusion HPLC) were lower in the patients with CLD (13 +/- 5 vs 21 +/- 2 nmol/l; P < 0.0001). Multiple regression analysis showed that GH secretion rate was increased in patients with CLD with higher Child's classifications (R2 = 0.86; P = 0.002) and with lower serum IGF-I concentrations measured after HPLC (R2 = 0.11; P = 0.044). CONCLUSIONS: Adults with chronic liver disease have (1) increased total daily GH secretion rates, which appear to be influenced by disease severity and diminished serum IGF-I-mediated negative feedback; (2) markedly impaired endogenous GH clearance, possibly reflecting changes in hepatic GH-receptor status; and (3) GHBP levels which do not correlate with GH kinetics or serum IGF-I concentrations.

Adult↗
PubMed1995

Genetic mapping of the multiple endocrine neoplasia type 1 locus at 11q13.

Oncogenesis of tumours related to multiple endocrine neoplasia type 1 (MEN1) is associated with somatic deletions involving the MEN1 locus at chromosomal region 11q13, suggesting inactivation of a tumour-suppressor gene in this region. Here we describe the localization of the MEN1 gene to a 900-kb region, based on linkage analysis in affected families and deletion mapping of MEN1-associated tumours. In addition, a set of microsatellite markers mapped to the 11q11-13 region were used for linkage analysis in a large Tasmanian MEN1 pedigree, demonstrating the usefulness of these markers for presymptomatic testing in affected families.

Adult↗
PubMed1995

Familial periodic cerebellar ataxia without myokymia maps to a 19-cM region on 19p13.

Familial periodic cerebellar ataxia (FPCA) is a heterogeneous group of rare autosomal dominant disorders characterized by episodic cerebellar disturbance. A potassium-channel gene (KCNA1) has been found to be responsible for one of its subgroups, familial periodic cerebellar ataxia with myokymia (FPCA/+M; MIM 160120). A different subgroup that is not associated with myokymia (FPCA/-M; MIM 108500) was recently mapped to chromosome 19p. Here we have performed linkage analysis in two large families with FPCA/-M that also demonstrated neurodegenerative pathology of the cerebellum. Three markers in 19p13 gave significant lod scores (> 3.0), while linkage to KCNA1 and three known loci for spinocerebellar ataxia (SCA1, SCA2, and SCA3) was excluded. The highest lod score was obtained with the marker D19S413 (4.4 at recombination fraction 0), and identification of meiotic recombinants in affected individuals placed the locus between the flanking markers D19S406 and D19S226, narrowing the interval to 19 cM. A CAG trinucleotide-repeat expansion was detected in one family but did not cosegregate with the disease.

Cerebellar Ataxia↗
PubMed1994

Multiple endocrine neoplasia type 1 (MEN1) in two Asian families.

Multiple endocrine neoplasia type 1 (MEN1), an autosomal dominant disease characterized by neoplasia of the parathyroid glands, anterior pituitary and endocrine pancreas, is rarely reported in Asian populations. The MEN1 gene, mapped to chromosome 11q13 but yet to be cloned, has been found to be homogeneous in Caucasian populations through linkage analysis. Here, two previously unreported Asian kindreds with MEN1 are described; linkage analysis using microsatellite polymorphic markers in the MEN1 region was carried out. The first kindred, of Mongolian-Chinese origin, is a multigeneration family with over 150 living members, eight of whom are affected to date. The second kindred is of Chinese origin consisting of four affected members. Linkage to chromosome 11q13 was confirmed in both kindreds, supporting evidence for genetic homogeneity. A recombination in the larger kindred localizes the gene distal to marker D11S956, consistent with its placement from previous studies. We also show that it is feasible to use these markers for predictive testing, as four gene carriers were detected in 13 family members with unknown disease status in the first kindred.

Adult↗
PubMed1994

The phospholipase C beta 3 gene located in the MEN1 region shows loss of expression in endocrine tumours.

Oncogenesis of tumours related to multiple endocrine neoplasia type 1 (MEN1) is associated with somatic deletions involving the MEN1 locus, suggesting inactivation of a tumour suppressor gene in this region. Identification of meiotic cross-overs in MEN1 families has placed the MEN1 locus centromeric of D11S807. An extended deletion mapping was performed in 27 primary parathyroid tumours, and identified D11S427 as the closest centromeric flanking marker. Through physical mapping using newly isolated cDNA clones, we estimated the distance between the flanking markers D11S807 and D11S427 to be less than 900 kb. One of these cDNA clones showed expression of a 4.4 kb message in multiple tissues, including those affected in MEN1, while in five endocrine tumours no transcript was detected. Sequence characterization showed that this gene encodes for the phospholipase C beta 3, a key enzyme in signal transduction.

Blotting, Northern↗
PubMed1994

Familial testicular carcinoma: in search of genetic triggers.

Two cases of testicular tumours in non-twin brothers of a cancer-prone family are described. Cytogenetic studies of these two patients and human leucocyte antigen (HLA) typing of the family failed to identify any genetic defects. The authors propose using linkage analysis for further genetic studies but would require additional families for this to be performed.

Adult↗
PubMed1993

Cause of death in multiple endocrine neoplasia type 1.

OBJECTIVE: Little data are available on the natural history of untreated multiple endocrine neoplasia type 1 (MEN-1). These data are essential in deciding treatment that may carry significant morbidity. We determined the causes of death in a large MEN-1 kindred with data available over a period of 130 years. Most cases were unrecognized as MEN-1 at the time of patient's death. DESIGN: Retrospective study of recorded medical data from 1861 to 1991. PATIENTS: One hundred fifty-nine deaths occurred, of which 46 were in individuals classified as "highly probable" of having MEN-1. RESULTS: Of 46 deaths in those classified as "highly probable" of having MEN-1, 20 (43.5%) died of a recognized complication of MEN-1 (12 of malignant neoplasms, six of renal calculi, and two of peptic ulcer). If accidental deaths are excluded, 50% of the deaths in patients with MEN-1 were the result of MEN-1, and the mean age of death (50.9 years)was significantly younger than that of other family members. CONCLUSIONS: It is concluded that MEN-1 leads to premature death, and that neoplasia rather than peptic ulcer disease is the main cause of death. Deaths from pituitary tumor or malignant endocrine tumors within the thorax were just as common or more common than deaths from pancreatic malignant neoplasms.

Adult↗
PubMed1993

Multiple endocrine neoplasm, type 1. Gastrinomas, pancreatic neoplasms, microcarcinoids, the Zollinger-Ellison syndrome, lymph nodes, and hepatic metastases.

OBJECTIVE: We reviewed the age of presentation, malignant potential, and outcome of gastrinomas and pancreatic tumors in patients with multiple endocrine neoplasm, type 1. DESIGN: Screening of one very large and one smaller, possibly related family on an island, including serum gastrin estimations and, when indicated, pancreatic ultrasound. SETTING AND PATIENTS: Over 2000 family members and their family physicians were advised on screening procedures. INTERVENTION: Data were collected and reviewed retrospectively and prospectively for all medical records, investigations, surgical procedures, and available tissue samples. OUTCOME MEASUREMENTS: Criteria for diagnosis were established for radiological, biochemical, and histological studies. RESULTS: Sixty-two patients had evidence of gastrinoma or pancreatic neoplasm. In 19 patients the diagnosis was based on demonstration of a tumor. In 21 patients the diagnosis was based on elevated serum gastrin concentration in the absence of demonstrable tumor. None of these patients required gastric surgery if they first underwent parathyroidectomy. In 18 patients the diagnosis was based on the combination of demonstrated pancreatic tumor plus elevated glucagon (two patients), gastrin (11 patients), or insulin (five patients) concentration. Peptic ulcer was difficult to control in seven of the 11 patients with elevated gastrin concentrations plus demonstrated tumor. Four patients had liver metastases that appeared to be secondary to the pancreatic gastrinoma. In patients with insulinomas, the first symptoms occurred before age 20 years. Elevated serum gastrin concentrations were not seen before age 24 years and were observed to occur for the first time in two patients after age 50 years.

Adolescent↗
PubMed1992

Hyperparathyroidism with normal albumin-corrected total calcium in patients with multiple endocrine neoplasia type 1.

In the largest reported family of patients with multiple endocrine neoplasia type 1 (MEN 1), hyperparathyroidism was expressed at first screening in 33 patients by elevation of ionized calcium (IC) (30 cases) or parathyroid hormone (three cases) without elevation of albumin-corrected total calcium (ACTC). Three of these 33 patients have shown a progressive rise in IC and later an elevation of ACTC. However, the age distribution suggests that in others the level of IC may remain stable at a minimally elevated level throughout life with ACTC remaining normal except for transient rises at the times of intercurrent illness or surgical operation. Even when ACTC is normal preoperatively, patients with an elevation of IC require radical subtotal parathyroidectomy or total parathyroidectomy and forearm implantation to restore IC to a normal level. Institutions that rely on ACTC as a screening test for hyperparathyroidism in MEN 1 will miss the diagnosis in nearly half of patients under the age of 30. The greatest deficiency in using ACTC occurs in the follow-up of patients who have undergone parathyroidectomy for MEN 1. Only three of 11 recurrences were evidenced by this measurement.

Adolescent↗
PubMed1991

Single base mutation in the hormone binding domain of the thyroid hormone receptor beta gene in generalised thyroid hormone resistance demonstrated by single stranded conformation polymorphism analysis.

Thyroid hormone resistance is a syndrome of considerable clinical heterogeneity. Three mutations in the c-erb A beta gene encoding the human beta thyroid hormone receptor have been described in different kindreds. We report here, in a family affected with peripheral thyroid hormone resistance, a unique point mutation in the ligand binding domain of the c-erb A beta gene resulting in histidine replacement of an arginine residue at position 438. The region in which the mutation occurred was identified by single stranded conformation polymorphism analysis and confirmed by subcloning and sequencing of the mutant alleles from each of the affected members. Binding of tri-iodothyronine to isolated nuclei from family members was normal suggesting the mechanism of thyroid hormone resistance in this family is not mediated by abnormal binding of ligand and receptor.

Adult↗
PubMed1991

Tussive effect of a fentanyl bolus.

The aim of this study was to investigate the incidence of pre-induction coughing, after an iv bolus of fentanyl. The study sample was 250 ASA physical status I-II patients, scheduled for various elective surgical procedures. The first 100 were randomly allocated to receive 1.5 micrograms.kg-1 fentanyl via a peripheral venous cannula (Group 1), or an equivalent volume of saline (Group 2). Twenty-eight per cent of patients who received fentanyl, but none given saline, coughed within one minute (P less than 0.0001). The second 150 patients were then randomly assigned to three equal pretreatment groups. Group 3 received 0.01 mg.kg-1 atropine iv one minute before fentanyl. Groups 4 and 5 received 0.2 mg.kg-1 morphine im, and 7.5 mg midazolam po, respectively, one hour before fentanyl. Thirty per cent of patients in Group 3, 6% in Group 4, and 40% in Group 5, had a cough response to fentanyl. Fentanyl, when given through a peripheral cannula, provoked cough in a considerable proportion of patients. This was not altered by premedication with atropine or midazolam, but was reduced after morphine (P less than 0.01). Coughing upon induction of anaesthesia is undesirable in some patients, and stimulation of cough by fentanyl in unpremedicated patients may be of clinical importance.

Adult↗
PubMed1979

Why do skin grafts fail?

Fibrin is shown to be the agent responsible for the adherence of biological dressings and of autografts to wounds. Its presence is associated with graft success, and its absence with graft failure. The results suggest that the deposition of fibrin provides the basis for the anti-bacterial actions of biological dressings and for the sterilization of the wound under adherent autografts. The total number of bacteria per gram of tissue in the wound, though important, is not critical to the result of skin grafting. The mechanism by which different organisms cause grafts to fail is by the production of plasmin and proteolytic enzymes which dissolve the important fibrin scaffold--thus ensuring their own survival. Thus, it is the levels of these (and the numbers of organisms efficient in producing them) which cause success or failure of applied skin grafts.

Aged↗
PubMedDate not supplied

Tumor suppressor genes (TSG).

In the last two decades the field of tumor suppressor genes (TSG) has developed from a novel epidemiology-based concept into one of the pillars of cancer research. New TSG are being discovered and although at a painstakingly slower pace, their functions are also being unravelled. These breakthroughs have not only brought about immediate benefits to clinical medicine such as genetic predictive testing for familial cancer syndromes, but have also introduced new strategies against cancer including early intervention, prevention and promising anti-cancer drugs. Despite that, we are still far from fully understanding the functional complexity of TSG with each discovery leading to even more queries. New developments that challenge the paradigm of TSG have also surfaced warranting verification and there is still a lack of consensual criteria and systematic cataloging for TSG. With the advent of high throughput sequencing and powerful bio-informatics, it is expected that the field of TSG will be expanding at an even faster pace. This review is to give a summary of the history, new concepts and recent advancements in the field of TSG in the hope that some of these concepts and works can be evaluated, expanded or even challenged.

Cell Transformation, Neoplastic↗