Biomedical subjects
Publications and source records attributed to R Jenkins.
Home healthcare nurses are encountering more medically at-risk children. In these situations, parenting roles and the responsibilities of the nurse are important. The concept of parents' grieving the loss of the "fantasy" child, the purpose of various grief feelings, and suggested nursing interventions in this situation are explored.
In this article a conceptual model for the study of child development in minority populations in the United States is proposed. In support of the proposed model, this article includes (a) a delineation and critical analysis of mainstream theoretical frameworks in relation to their attention and applicability to the understanding of developmental processes in children of color and of issues at the intersection of social class, culture, ethnicity, and race, and (b) a description and evaluation of the conceptual frameworks that have guided the extant literature on minority children and families. Based on the above considerations, an integrative conceptual model of child development is presented, anchored within social stratification theory, emphasizing the importance of racism, prejudice, discrimination, oppression, and segregation on the development of minority children and families.
The gene encoding the cell cycle inhibitor p16INK4A (also known as p16, MTS1, CDKN2 and INK4) has been mapped to human chromosome band 9p21, a region that also contains a putative melanoma susceptibility gene. Although germline mutations in the coding region of the p16INK4A gene have been detected in some families with inherited melanoma, many other families show no evidence of such mutations and hence the role of p16INK4A in the development of this tumor is still unclear. In this report, we describe a family with inherited melanoma in which a novel mutation in exon 2 of the p16INK4A gene segregates with the disease. The mutant gene encodes a protein with an in-frame deletion of two amino acids (Asp96 and Leu97). We show that the mutant protein is functionally abnormal: it is unable to bind cdk4 in vitro and does not inhibit colony formation in tertiary passage rat embryo fibroblasts. Moreover, in a metastatic lesion from one patient the wild type p16INK4A allele was deleted and the mutant allele retained. We conclude that family members carrying this germline mutation in the p16INK4A gene are predisposed to melanoma. By extension, these findings implicate the p16INK4A gene in the development of some cases of familial melanoma.
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Human hepatocyte viability and function in vivo in an athymic rat was assessed after transplantation on prevascularized polymer constructs with hepatotrophic stimulation. Sixteen liver biopsy specimens, weighing 5 to 12 g, were obtained from the New England Organ Bank and from the operating room after liver resection. In the laboratory they were catheterized and perfused to obtain liver cell suspensions. From eight of the 16 cell suspensions, only in vitro studies were performed. They showed 40% cell attachment 24 hours after initial cell plating. For patients aged 2, 35, and 60 years, they showed a 20% increase, a 1% decrease, and a 57% decrease (respectively) in cell number from day 2 to day 4, after cell plating. Eight cell suspensions were transplanted into athymic rats. On sections examined histologically, implanted hepatocytes were seen within the fibroblast ingrowth, in the space of the polymer device, until day 21 after cell injection. On day 9 after hepatocyte injection, reorganized hepatic parenchyma was seen on the tissue section. Implanted hepatocyte areas, quantitated through morphometric analysis on days 0, 3, and 7, showed a 36% increase in engraftment 3 days after injection, and a 42% decrease 7 days after injection. At the same time-points, immunoperoxidase staining visualized intracellular albumin, which was specific for the implanted hepatocytes. In conclusion, the authors demonstrated the feasibility of their technique (prevascularized polymer device with hepatotrophic stimulation), using human hepatocytes. Further studies are underway, before implementation of human clinical trials.
PURPOSE: Williams syndrome is a rare genetic disorder, consisting of mental retardation, supravalvular aortic stenosis, elfin facies, and specific ocular findings, including strabismus. We undertook this study to evaluate the characteristics of the strabismus in Williams syndrome. METHODS: We examined 32 patients with Williams syndrome to determine the prevalence and define the features of the strabismus in this patient population. RESULTS: Twenty-five of the 32 patients (78%) had strabismus, esotropia being the predominant form in 23 of the 25 patients. Of the 19 patients with Williams syndrome who had infantile esotropia, seven had dissociated vertical deviation, ten had oblique dysfunction, and six had amblyopia. CONCLUSIONS: When the patients with Williams syndrome were compared to the general population, no statistically significant difference was found in the clinical characteristics of infantile esotropia between the two groups. Because of the high prevalence of esotropia in patients with Williams syndrome (72%) compared to the general population (0.1%), we postulate a genetic link between Williams syndrome and the hereditary form of infantile esotropia.
We present the results of a retrospective review of abdominal computed tomography, ultrasound, and magnetic resonance examinations of 12 patients with primary biliary cirrhosis undertaken to determine the prevalence and clinical significance of previously reported coexistent intra-abdominal lymphadenopathy in patients with this disorder. Lymphadenopathy, in the form of bulky periportal and retroperitoneal nodes, was identified in a single patient secondary to an occult metastatic adenocarcinoma. We conclude that coexistent intra-abdominal lymphadenopathy occurring in patients with primary biliary cirrhosis is uncommon. Although it may represent a benign component of the primary disease, it may equally be due to unsuspected coexistent occult malignancy.
Many tumour types have been reported to have deletion of 9p21 (refs 1-6). A candidate target suppressor gene, p16 (p16INK4a/MTS-1/CDKN2), was recently identified within the commonly deleted region in tumour cell lines. An increasing and sometimes conflicting body of data has accumulated regarding the frequency of homozygous deletion and the importance of p16 in primary tumours. We tested 545 primary tumours by microsatellite analysis with existing and newly cloned markers around the p16 locus. We have now found that small homozygous deletions represent the predominant mechanism of inactivation at 9p21 in bladder tumours and are present in other tumour types, including breast and prostate cancer. Moreover, fine mapping of these deletions implicates a 170 kb minimal region that includes p16 and excludes p15.
Following two previous articles which described changes that are occurring in suicide rates and trends in factors known to be associated with suicides, this article examines in greater depth the effect of occupation and geography on suicide mortality. For both men and women the highest risk occupations are mostly in Social Class I or II. The occupations at highest risk, which include several medical-related professions, and the method of suicide they choose, suggest that easy access to means of suicide is an important factor. Suicide rates for men aged 15-44 are generally higher in Inner London, rural areas, resort and retirement areas, and urban manufacturing areas.
BACKGROUND: Most mental illness is treated in primary and not secondary care settings, with depression and anxiety the commonest conditions encountered. METHOD: The paper describes on-going Department of Health initiatives to optimise the primary care of common mental illnesses such as depression. DISCUSSION: Primary care attenders with depression are often higher consumers of general health care than non-depressed attenders. Further data will become available soon from these ongoing studies to inform the debate on the optimal use of available resources in primary care. There is a particular need to evaluate non-pharmacological interventions in primary care.
The primary aim of this report was to examine the significance of increased DNA sequence copy number (gene amplification) in human prostate cancers. Three methodologies (chromosome microdissection, comparative genomic hybridization, and fluorescence in situ hybridization) were combined to (a) identify a common region of gene amplification in human prostate cells and (b) evaluate in patient samples the prevalence of this genetic change in both primary and recurrent prostate samples. The results of chromosome microdissection revealed a common amplified band region (8q24.1-24. 2) in two prostate cases with cytological evidence of gene amplification (double minutes). Fluorescence in situ hybridization using the 8q microdissection probe was performed on fresh tumor touch preparations from 44 randomly selected prostatectomy specimens. Amplification of DNA sequences from 8q24 was observed in 4 (9%) of 44 cases. Four of the 44 patients in this series presented with a positive lymph node at initial diagnosis and 3 of these 4 patients showed 8q amplification. Because of this finding, comparative genomic hybridization and fluorescence in situ hybridization were performed on tumor cells from nine prostate cancer patients with recurrent disease. In eight of nine cases a gain of DNA sequences encompassing 8q24 was observed. Taken together with other evidence implicating 8q gain in prostate cancer progression, these results suggest that the analysis of this genetic change may have diagnostic utility as a marker of prostate cancer progression.
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Because of the almost universal recurrence of hepatitis B surface antigenemia (HBsAg) after liver transplantation, some centers have questioned whether these patients are appropriate allograft candidates. Since January 1984, 51 patients with hepatitis B (HBV) underwent OLT at our center. No therapy was given to prevent reinfection. Three patients underwent retransplantation. The indications for transplant included fulminant HBV (13 patients), chronic HBV (33 patients), and hepatocellular carcinoma (HCCA) in addition to HBV (5 patients). Incidental HCCA was found in 2 of the 33 patients thought to have only chronic HBV. Actuarial survival for the entire group was 57% at 1 year and 54% at 3 years. Of the 23 patients who died, only 4 deaths were attributable to recurrent HBV liver disease. Four patients survived less than 4 days due to primary graft nonfunction. Ten patients died in the first 3 months from sepsis. Although all patients who died beyond 30 days had recurrent HBsAg, only 4 deaths were attributable to recurrent HBV. The remaining 5 deaths were caused by portal vein thrombosis, bile leak, lymphoma, pancreatitis, and sepsis occurring at 15 months. Excluding the 4 patients who died from primary graft nonfunction, actuarial survival was 63% at 1 year and 60% at 3 years. Of the 28 survivors, 24 are HBsAg positive; however, only 5 have recurrent HBV liver disease. Multiple factors were evaluated to determine their influence on survival; i.e., HBV serology, United Network for Organ Sharing status, fulminant versus chronic HBV, incidence of rejection, immunosuppression, transfusion requirements, and presence of HCCA. Of these, only the presence of HCCA adversely affected outcome. Of the 7 patients with HCCA and HBV, 6 patients died within the first 6 months and 1 patient has recurrent HBV liver disease at 25 months. Actuarial survival excluding those patients with HCCA was 64% at 1 year and 61% at 3 years. Based on our results, patients with HBV and associated HCCA have a poorer prognosis and should probably be excluded from transplantation. Although the survival for patients with HBV undergoing liver transplantation is inferior to that expected in patients with some other diagnoses, long-term survival can be achieved in a majority of these patients despite recurrence of HBsAg. We believe that appropriately selected patients with a diagnosis of HBV alone should continue to be candidates for liver allografts.
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Earlier studies have clarified the sequence and control of behavioral interactions during nursing in the rat. For comparison, we analyzed nursing behavior in the precocial guinea pig (Cavia porcellus). The behaviors of 6 dams with litters of 3 pups were videotaped under undisturbed conditions during both phases of the light-dark cycle and after reunion during the light phase on Days 1, 2, 3, 6, and 13 postpartum. More time was spent nursing in the light than in the dark and in the 1st week than on Day 13. Pup licking was not required for nipple attachment to occur even on Day 1. Dams displayed a crouched nursing posture accompanied by 120 s or more of body plus head immobility, similar to the crouched stance in the rat; body plus head immobility was rarely seen in females not in a crouched stance.
The case of a patient who developed remarkably extensive tumid nodules and plaques in a cobblestone pattern on the extensor aspects of the limbs is reported as a late presentation of captopril-induced lichenoid eruption. The severity and chronicity of our patient's symptoms and signs reflected delay in reaching the diagnosis.