Biomedical subjects
Publications and source records attributed to P Watson.
Augmentation of the acetabular component of total hip replacements is a method of increasing stability and preventing recurrent dislocation. We report a series of mechanical experiments designed to evaluate the turning moments and angles required to dislocate standard, long posterior wall and two different augmented prostheses.
Throughout the ages, physicians have listened to sounds and felt vibrations from human joints in their attempts to diagnose pathology. They have used a wide vocabulary to describe these phenomena, but technology has been slow to provide recording and analytic equipment. Lately, accelerometers have been used with considerable success in a new noninvasive method now known as vibration arthrometry (formerly "arthrography"). The technique has been used in early detection of congenital dislocation of the hip and also in diagnosis of meniscal pathology. More recently, patellar vibration has been used to assess the mechanical properties of articular cartilage. Vibration arthrometry has also yielded new information on a possible damage mechanism associated with shock vibration that arises during cavitation of synovial fluid. Joint vibrations are therefore useful aids to diagnosis and may even be etiologic in orthopedic disease.
Host factors have been given scant attention in the search for etiology in pancreatic cancer. Several anecdotal reports have identified its familial clustering, whereas a recent population-based case/control study has shown that 6.7% of cases and 0.7% of controls had positive family histories of this disease (p less than 0.001). Forty-seven individuals with pancreatic cancer from 18 families were identified from a review of the medical records of all kindreds on file at our Hereditary Cancer Institute. The observed sex ratio, age of onset, histologic type, and survival were comparable to published data on unselected patients. We did not identify any pattern of extra-pancreatic cancer association. A serious limitation of our study is its lack of a population-based case/control design. Whereas our data are primarily descriptive, they do indicate the need to learn more about the role of familial factors in the etiology of pancreatic cancer. Pancreatic cancer is increasing in incidence, and its prognosis is almost uniformly dismal; identification of persons at high risk may improve cancer control.
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We have studied a remarkable family with seven cases of malignant lymphoma extending through three generations wherein five sisters and their mother had histopathologically documented non-Hodgkin's lymphoma, while a granddaughter had Hodgkin's disease. An immunological study of three lymphoma survivors, nine of their first degree relatives, and four spouse controls was undertaken. Significant findings consisted of a depressed serum IgG3 level in four of the nine first-degree relatives; in two of these four, lymphocyte stimulation by both pokeweed mitogen and concanavalin A were significantly depressed. The subtle immunological abnormalities present in this kindred may be associated with the pathogenesis of the lymphomas.
HBC is common, accounting for approximately 9% of the total breast cancer burden. Given 142,000 cases of breast cancer expected to occur in 1989, this would represent 12,780 cases of HBC patients. Soberingly, each patient represents a family with a variable number of inordinately high risk patients. HBC's natural history is distinctive and enables the identification of at risk patients who can benefit from highly targeted surveillance/management strategies. High priority must be given to development of biomarkers that will one day be found to have acceptable sensitivity and specificity to genotype status. Thus, we would then be able to tell which of the first-degree relatives of affected members have inherited the deleterious gene. This would result in a significant saving of time and money that would otherwise be expended through intensive surveillance strategies. We need cost-benefit research to induce third party carriers to defray expenses for surveillance. Finally, priority attention must be given to biomolecular research for identification of markers of acceptable sensitivity and specificity to the cancer-prone genotype. Eventual cloning of the deleterious gene(s) could lead to knowledge about its chemical and physiologic products, thereby enabling anticancer pharmacologic research. The reward could then be improved control and even prevention of breast cancer, and possibly of the associated cancers in heterogenous forms of this disease.
The familiar cracking sounds produced by distraction of the metacarpophalangeal joints were studied using accelerometers and a computerized signal analysis system. The joints were distracted in a controlled manner using a motorized device which simultaneously monitored the load on the joint and its extension. The load and extension parameters and those from the signal analysis were used to examine diurnal variation, the effects of multiple distractions, distraction speed, hand temperature and loading between distractions, and to show that in many cases, the energy contained in a crack signal, expressed as a ratio of the articular cartilage volume, exceeded a known level needed to produce articular cartilage damage.
There is a significant hiatus between existing knowledge about hereditary forms of cancer and the application of this information at the bedside. We believe that the HCCC concept will effectively bridge this gap between medical knowledge and its service application. Priority areas for assuring long-range success of this mission will require: a) greater public and physician awareness of the hereditary portion of the total cancer problem; b) generation of cost-benefit information relevant to the surveillance and management of patients at risk for hereditary cancer so that third party carriers might be more responsive to patient needs: c) enhancement of patient/family compliance with surveillance/management protocols leading to early detection of cancer and improved survival; and d) research into biomarkers which demonstrate acceptable sensitivity and specificity for the cancer-prone genotype, one day enabling identification of the deleterious gene(s). Thus, we may achieve the ultimate goal of identifying biochemical agents which will effectively ameliorate the deleterious products of the cancer-prone gene(s), improve clinical outlook, or even prevent cancer expression.
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Cavitation, the term used to describe bubble activity in fluids, is a destructive phenomenon encountered in fluid systems. The effect of cavitation on articular cartilage was investigated by ultrasonically inducing bubble activity on the surface of bovine specimens. Distinctive pits and craters, not present on control specimens, were observed using scanning electron microscopy on the damaged surface. Human osteoarthrotic articular cartilage specimens were removed during arthroplasty and examined using scanning electron microscopy. Craters and pits observed on the osteoarthrotic specimens were similar in appearance to those on the cavitated specimens. The mechanism of cavitation bubble collapse could be responsible for damage in vivo, thus providing articular cartilage with a degenerative pathway toward osteoarthrosis.
Hereditary nonpolyposis colorectal cancer (HNPCC) accounts for about 4% to 6% of the total colorectal cancer burden. It is subdivided into Lynch syndrome I and II. Lynch syndrome I is characterized by an autosomal dominant inheritance pattern for site-specific, early onset, adenocarcinoma of the colon, with proximal predominance and an excess of synchronous and metachronous colonic cancers. Lynch syndrome II (cancer family syndrome) shows these same colon cancer characteristics, but differs in that there is an excess proclivity of other forms of cancer, particularly of the endometrium and ovary. This article documents a family that shows features of Lynch syndrome II. Unique aspects pertain to a patient who is in the direct genetic lineage (whose five brothers manifested colonic cancer), but who developed carcinoma of the uterine cervix at age 34 and laryngeal cancer at 60. The pedigree also shows uterine cervical carcinoma among other patients at genetic risk. Her son, who is a nonsmoker and nondrinker, manifested laryngeal cancer at age 31. These observations appear to add new information about tumor heterogeneity in HNPCC.
Since full breast cancer screening is not generally recommended for young women, it is important to identify individuals who are at higher risk for early onset breast cancer. We investigated the relationship between age of onset of breast cancer in 328 probands (consecutively ascertained patients from our oncology clinic) and breast cancer incidence and age of onset in their female relatives. We found that a family history of early onset breast cancer was associated with higher risk of early onset breast cancer. A family history of early onset breast cancer occurred more frequently among young (less than 40) breast cancer probands than among older (greater than or equal to 40) breast cancer probands (p less than 0.001; OR = 23). This relationship was particularly evident when the analysis was restricted to the hereditary breast cancer probands (p less than 0.001; OR = 44). We also observed a positive family history of breast cancer (any age) more frequently in young breast cancer probands than in older breast cancer probands (p less than 0.001; OR = 2.8). These observations have important pragmatic implications for surveillance. We recommend intense surveillance for breast cancer, initiated earlier, for women with close relatives diagnosed with early onset breast cancer.
Knowledge of the family history of cancer may significantly influence diagnosis and surgical management. Hereditary breast cancer (HBC) is common and accounts for approximately 9% of the total breast cancer burden. The pattern of HBC's natural history, including age of onset, increased incidence of bilaterality, integral tumor combinations in certain kindreds, and vertical transmission consonant with an autosomal dominantly inherited factor, when observed in context with the family history, enables pattern recognition so that the diagnosis might be facilitated. We describe seven families from our Hereditary Cancer Consultation Center (HCCC) and the Creighton Oncology Clinic which are noteworthy for extraordinarily early age of onset. This appears to be an additional example of heterogeneity in HBC and may represent the first account of this remarkable subset. The manner in which age of onset can be incorporated with other aspects of natural history for expediting diagnosis is discussed.
Approximately 5 to 6 percent of the total colorectal cancer burden is accounted for by hereditary nonpolyposis colorectal cancer (HNPCC). Because clinical premonitory signs such as those seen in familial polyposis coli (FPC) are lacking, the clinician must recognize clinical findings and family history typical of HNPCC. The authors have described colorectal cancer expression from a survey of ten HNPCC kindreds. Kindred members with colorectal cancer differed significantly (P less than .05) from patients with sporadic colorectal cancer: 1) mean age of initial colon cancer diagnosis was 44.6 years; 2) 72.3 percent of first colon cancers were located in the right colon, and only 25 percent were in the sigmoid colon and rectum; 3) 18.1 percent had synchronous colon cancers; and 4) 24.2 percent developed metachronous colon cancer, with a risk for metachronous lesions in ten years of 40 percent. Affecteds and their first-degree relatives should undergo early intensive education and surveillance. In families with an early age of onset, colonoscopy should begin at age 25, and biannually thereafter, with fecal occult blood testing of the stool semiannually. Third-party carriers must become more responsive to the costly surveillance measures required for these otherwise healthy patients.
Increasing recognition of the statistical burden posed by HNPCC (5 to 6 percent of all colorectal cancer) mandates that physicians have a better understanding of the genetics, natural history, and distinction between the hereditary site-specific variant (Lynch syndrome I) and the Cancer Family Syndrome (Lynch syndrome II). The authors report detailed cancer (all sites) family histories on two prototype families with Lynch syndrome I (Family R) and Lynch syndrome II (Family N), which have been under investigation for more than two decades. Emphasis is placed on shared clinicogenetic features; namely, early age of onset of colonic cancer (approximately age 44), multiple primary colonic cancer (24 percent of cases showed metachronous colonic cancer), predominance of proximal colonic cancer location (approximately 65 percent in the proximal colon), and vertical transmission consonant with an autosomal dominantly inherited factor. An increased predilection for extracolonic cancer, particularly endometrial carcinoma, occurs in Lynch syndrome II and is the primary basis for distinction from Lynch syndrome I. Surveillance and management programs must be wholly responsive to these natural history features.
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