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Biomedical subjects

J P Farrell

Publications and source records attributed to J P Farrell.

50 records · Page 3Linked to original sources
PubMed1982

Acute low back pain. Comparison of two conservative treatment approaches.

In a controlled clinical trial, we allocated 48 subjects with acute low back pain but without neurological signs, at random to two treatment groups. The conservative treatments compared were passive mobilisation and manipulation of the lumbar spine and a regimen of microwave diathermy, isometric abdominal exercises and ergonomic instructions. The duration of low back pain symptoms was significantly shorter for subjects receiving mobilisation and manipulation; they also achieved symptom-free status with fewer treatment sessions. While the duration of symptoms before first treatment, the treatment administered, and the pretest forward flexion movement indices accounted for 44% of the variance in the duration of symptoms, a stepwise multiple regression analysis showed that treatment is the most significant factor in predicting the length of time before a subject achieves symptom-free status.

Abdomen↗
PubMed1982

Pathogenesis of anaemia in hamsters infected with Leishmania donovani.

The development of anaemia was studied in hamsters infected with Leishmania donovani. Haematocrit studies as well as erythrocyte survival studies using radioactive chromium (51Cr), gave evidence of a progressive anaemia during the course of infection. The erythrocytes were positive in direct antiglobulin tests using antisera to IgG and complement C3. Moreover, erythrophagocytosis as well as increased deposits of haemosiderin in the liver and the spleen, particularly in the areas of proliferating macrophages, were demonstrated. It would appear that the erythrocytes adsorb immune complexes on their surfaces and become liable to enhanced phagocytosis by the macrophages of the liver and the spleen.

Anemia↗
PubMed1982

Leishmaniasis in beige mice.

The courses of two protozoal diseases, cutaneous and visceral leishmaniasis, were examined in three groups of C57BL/6J mice. One group of mice was homozygous recessive for the beige gene (bg/bg). Beige mice are the genetic homologue of the human Chédiak-Higashi syndrome and, among other defects, are profoundly deficient in natural killer cell activity. Wild-type (+/+) mice, which respond to experimental cutaneous or visceral leishmaniasis by eventually eliminating their parasites, and heterozygous beige (bg/+) mice served as controls; both are phenotypically normal in natural killer cell activity, which is particularly high in the spleen. In bg/bg mice, the course of Leishmania tropica, a causative agent of cutaneous leishmaniasis, was similar to that in control mice after both primary and challenge inoculations. All groups of mice expressed similar humoral and cellular immune responses to L. tropica antigen. However, bg/bg mice failed to eliminate amastigotes of Leishmania donovani, a causative agent of visceral leishmaniasis, from their spleens over an observation period of 56 days, in contrast to bg/+ and +/+ controls. Similar levels of anti-leishmanial antibody were produced by all groups of mice, and all mice responded comparably to footpad injections of L. donovani antigen. The results of this study suggest a possible role for natural killer cells in recovery from L. donovani but not from L. tropica infection.

Animals↗
PubMed1981

Single gene control of resistance to cutaneous leishmaniasis in mice.

A series of inbred, congenic resistant, and hybrid strains of mice were intradermally inoculated with 10(6) promastigotes of Leishmania tropica. These mice were divided into susceptible and resistant groups using the criteria of lesion size, development of metastatic foci and skin-test reactivity. At 16 weeks of infection, resistant strains A/J, DBA/1J, AKR/J, CBA/J, C3H/HeJ, NZB/BINJ, C57BL/6J, C57BL/10Sn, B10.D2, B10.129(10M), and B10.CE(30NX) had completely resolved their lesions, while susceptible SWR/J and BALB/cJ mice demonstrated large, nonhealing cutaneous lesions. In addition, BALB/cJ developed metastatic lesions on the extremities which progressively increased in size. A11 BALB/cJ and SWR/J mice died by 7 1/2 months of infection. The BALB/cJ female x C57BL/6J male F1 hybrid behaved in an intermediate fashion showing a slower expansion of cutaneous ulcers and a delayed development of metastatic foci, however, the infection ultimately proved fatal. The F2 generation could be separated into three distinct groups:resistant, intermediate, and susceptible mice with a lesion size distribution pattern in conformity with a 1:2:1 ratio. Male/female susceptibility differences were not noted. These data indicated that development of acquired resistance may be under the control of a single, autosomal gene. The gene did not appear to be H-2-, Ir-2-, or H-11-linked as is seen with Leishmania donovani infections.

Animals↗
PubMed1981

Experimental cutaneous leishmaniasis. I. Nonspecific immunodepression in BALB/c mice infected with Leishmania tropica.

Leishmania tropica in BALB/c mice causes a fatal infection accompanied by the development of multiple metastatic lesions. Spleen cells from these mice were shown to have depressed proliferative responses to concanavalin A (Con A), phytohemagglutinin (PHA), and lipopolysaccharide (LPS). Coinciding with this immunodepression was the development of a cell population capable of suppressing normal spleen cell responses to Con A. This suppressor cell activity was first observed at 6 wk and was present throughout the remainder of the infection. At 12 wk the suppressor cells could be removed by Sephadex G-10 passage or carbonyl iron treatment; however, Sephadex G-10 passage could not reverse the suppression at 18 wk. Indomethacin, a prostaglandin synthetase inhibitor, was found to abrogate the activity of the adherent suppressor cell, suggesting that prostaglandin production may be involved in the immunosuppression seen in these mice. In addition, Sephadex G-10 passage and indomethacin were found to markedly augment spleen cell responses to leishmanial antigen, indicating that the adherent suppressor cell is capable of regulating specific immunologic responses.

Animals↗
PubMedDate not supplied

Back school programs. The young patient.

CC's treatment goals were all met with the exception of eliminating the AMNT sign. Slump-sit right knee extension (-15 degrees), right SLR (80 degrees coupled with dorsiflexion), and lumbar flexion (85% coupled with neck flexion) all continued to reproduce right buttock cramping and pain. Currently he is playing basketball without restriction, performing an individualized exercise program that emphasizes lower extremity muscle stretching, AMNT stretching, and advanced truncal stabilization exercises. He has a very good understanding of body mechanics and an awareness of safe SFP during activities of daily living and on the basketball court. His motivation, along with the motivation of parents, coaches, athletic trainer, and physical therapist, greatly assisted CC in returning to competitive basketball. CC is intermittently evaluated to monitor the AMNT sign and the effectiveness of the home exercise program. Currently CC's AMNT appears to regress if he is not monitored on a monthly basis; thus he warrants intermittent treatment. Monitoring of the patient is an integral aspect of long-term management of chronic discogenic disease that is often neglected. It can be hypothesized that monitoring may prevent serious complications in the future for many patients. CC is a patient who needed specific therapeutic intervention beyond rest, general instructions about body mechanics and exercise, modalities, and traditional back school. The history of this patient's problem revealed that rest and general exercises had failed, thus necessitating specific therapeutic treatment. This patient is an excellent example of how physical therapy in the form of manual therapy, specific therapeutic exercise, education through repetition of functional tasks, and the team approach to patient care can lead to a successful treatment outcome.

Adolescent↗