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Biomedical subjects

J Nieves

Publications and source records attributed to J Nieves.

48 records · Page 3Linked to original sources
PubMed1991

Motor evoked potentials elicited from pyramidal stimulation and recorded from the spinal cord in the rat.

This study investigated the spinal evoked response to focal electrical stimulation of the sensorimotor cortex in 32 rats. The results demonstrate a long-latency response (beginning at 8 milliseconds) elicited by electrical stimulation, which is distinct from the short-latency motor evoked potential previously reported. The conduction velocity of this later response is similar to that reported for the pyramidal tract in the rat. Experiments confirm that the longer latency response depends upon the integrity of the pyramidal system. Focal stimulation outside the sensorimotor cortex failed to elicit a response. Experimental lesions of the pyramidal tract or ablating the sensorimotor cortex eliminated the spinal cord evoked response. The results demonstrate that focal stimulation of the sensorimotor cortex results in a spinal cord evoked response that represents activity within the pyramidal system. The utility of this response in the rat model for assessing experimental cord injury is discussed.

Animals↗
PubMed1991

The effects of spinal gray activation by strychnine on the motor evoked potential in the rat.

Spinal motor evoked potentials were elicited by electrical stimulation of the motor cortex in 14 rats before and after the application of strychnine to the surface of the spinal cord. Strychnine applied to the high cervical cord resulted in the emergence of additional peaks at the site of application and in electrodes positioned distally on the middle and lower thoracic cord. The strychnine-induced peaks occurred earlier and were larger in amplitude (P less than 0.01) in the distal spinal cord. Strychnine applied to the lower thoracic cord resulted in similar peak generation in the lower thoracic cord and in the spinal cord proximal to the application of strychnine. These findings demonstrate that strychnine-induced motor evoked potential changes arise from spinal gray activity induced by efferent pathways activated during transcortical stimulation. The role of the propriospinal tract in mediating the distal effects of strychnine is discussed. In conclusion, the strychnine-induced peaks of the motor evoked potential may be used as a measure of spinal gray integrity in experimental spinal cord injury models.

Animals↗
PubMed1991

CNS activation patterns underlying motor evoked potentials as demonstrated by c-fos immunoreactivity.

Monopolar (n = 5) and bipolar (n = 4) electrical stimulation of the motor cortex associated with spinal motor evoked potentials (MEPs) in rats resulted in central nervous system (CNS) staining for c-fos protein. Staining was demonstrated in the cortex, hippocampus, and caudate-putamen, irrespective of the type of stimulation. C-fos protein was demonstrated in the ventral horn cells in 3 animals and in the superficial layer of the posterior horn in 8 animals. Brainstem staining was more frequent and intense in rats stimulated with monopolar electrodes. In contrast to the diffuse and bilateral cortical staining observed with electrical stimulation, motor cortex stimulation by the local application of bicuculline resulted in c-fos protein staining restricted to the stimulated motor cortex. The cerebellum failed to demonstrate c-fos protein following motor cortex stimulation or direct electrical cerebellum stimulation. The present study demonstrates that c-fos protein can be used as a marker of direct or synaptically activated neurons during electrical and chemical stimulation of the motor cortex. Activation of neural structures outside the motor pathway may reflect physiologic activation or stimulus spread. Increased c-fos protein staining of the brainstem with monopolar stimulation supports previous studies that suggest that components of the MEP following monopolar motor cortex stimulation in the rat may arise from brainstem structures.

Animals↗
PubMed1990

Postgraduate internship in gynecology and obstetrics for physician assistants: a 4-year experience.

Changes in the Hospital Code (405 Regulations) to limit the number of hours worked by residents have been implemented in New York state and may soon become a nation-wide policy. Although their goal is to guarantee quality of patient care and assure education for residents, the limitation of hours worked has increased manpower shortages, some of which could be resolved by using physician assistants with specialty training. To provide this training, a Postgraduate Internship in Gynecology and Obstetrics for Physician Assistants has been developed at the North Central Bronx Hospital and the Montefiore Medical Center. It is the first program of its kind at the postgraduate level to educate physician assistants specifically for practice in obstetrics and gynecology. The program consists of 3 months of didactic lectures to review and update knowledge on topics in medicine, surgery, gynecology, preoperative and postoperative care, cardiac and trauma life support, and critical care, followed by a clinical year similar to that of a rotating physician intern. We believe that such postgraduate educational opportunities in gynecology and obstetrics benefit both the individual physician assistant's growth and development and the level of care delivered, and may be an answer to staffing needs.

Curriculum↗
PubMed1989

Systemic biodistribution of radioiodinated interleukin-2 in the rat.

Interleukin-2 (IL-2) is a lymphokine capable of modulating a variety of immune functions. In vitro and in vivo studies have shown promising cytotoxic potential. Despite numerous ongoing clinical trials, however, little is known about the biodistribution of this lymphokine after in vivo administration. In this study using a rat model, the fate of radioiodinated human recombinant IL-2 (RIL-2) was analyzed by camera imaging, autoradiography, and well counting experiments. Camera imaging demonstrated the liver and kidney to be the organs of greatest radioactivity accumulation with peak liver uptake noted at approximately 10 min from onset of infusion, and peak kidney uptake at approximately 20 min. Autoradiographic assessment of selected organs (kidney, adrenal, liver, lung, and brain) revealed marked heterogeneity of uptake in the kidney and adrenal gland with preponderance of RIL-2 in the cortex of these organs. A more homogeneous distribution of RIL-2 uptake was noted in liver, lung, and brain parenchyma. Well counting confirmed the liver and kidney as the organs of greatest RIL-2 accumulation. Knowledge of the biodistribution of IL-2 may be of benefit both in studying mechanisms of toxicity and in designing novel therapeutic approaches.

Animals↗
PubMed1987

Electron spin resonance of calmodulin-vanadyl complexes.

X-band (9.2 GHz) electron spin resonance spectroscopy was used to investigate the binding of vanadyl to calmodulin. Solution spectra, obtained at ambient temperature with various VO2+:calmodulin molar ratios, suggested a binding stoichioimetry of 4 mol of VO2+/mol of protein and the possibility of two classes of binding sites. The latter was confirmed by using frozen solutions of calmodulin-VO2+ complexes that gave splitting of the spectral bands corresponding to the parallel components, which was particularly pronounced with the three high-field peaks. Competition of Ca2+ for the VO2+ binding sites was investigated, and the results indicated that two of the VO2+ sites corresponded to two of the Ca2+ sites; the other two VO2+ binding sites may have a higher affinity for VO2+ than for Ca2+ or they may correspond to Ca2+-independent sites. These results demonstrate that electron spin resonance spectroscopy can be used advantageously to probe subtle differences in the microenvironments of metal-binding sites in calmodulin.

Binding Sites↗
PubMedDate not supplied

Possible regulation of high-affinity glutamate uptake in synaptosomes of normal and epileptic mice.

Glutamate (Glu) uptake is the primary mechanism for its removal from the synapse. In genetic audiogenic seizures (AGS), Glu uptake is elevated prior to the appearance of seizures. Increased Glu uptake is also observed in synaptosomes from normal mice preincubated with lithium or nitroarginine, an NO synthase inhibitor. Pertussis and cholera toxins cause a marked reduction in Glu uptake. In contrast, neither lithium nor nitroarginine affected Glu uptake by synaptosomes from genetic epileptic mice. Arachidonic acid inhibits Glu uptake, whereas synaptosomes from epileptic mouse brain appear to be more sensitive to arachidonic acid as indicated by a shift of the inhibition curve to the left. These observations are indicative of the possible regulation of Glu uptake by second messengers and its alteration in genetic epilepsy.

Acoustic Stimulation↗
PubMedDate not supplied

Differences in histology between first and second primary lung cancer.

Data from the Surveillance, Epidemiology, and End Results (SEER) Program were used to compare the histological distribution of second lung cancer following an initial cancer of the lung, head and neck, and breast to primary lung carcinoma occurring as a first cancer. Following initial head and neck cancer or initial squamous cell carcinoma of the lung, the proportion of second primary lung cancer which was of squamous cell histology rose dramatically, while the proportion of pulmonary adenocarcinomas rose following initial adenocarcinoma of the lung. The histological distribution of lung cancer following an initial breast cancer in women was similar to the distribution of de novo lung cancer in women. These results persisted as the time interval between diagnosis of the two primaries was increased from 12 to 48 months. We conclude that the histology of a second primary lung cancer following an initial cancer of the lung or head and neck tends to repeat the histology of the initial cancer (field effect), and this observation is not likely to be due to misdiagnosis of a recurrence of the initial cancer.

Adenocarcinoma↗
PubMedDate not supplied

Poor survival of treatment-related acute nonlymphocytic leukemia.

Population-based data on more than 1 million patients registered in the Surveillance, Epidemiology, and End-Results Program of the National Cancer Institute, 1973 to 1984, were analyzed to determine the survival of patients with de novo acute nonlymphocytic leukemia (ANLL) and following a first primary tumor treated (with chemotherapy and/or radiation therapy) or untreated. Cases that occurred within 12 months of the first malignant neoplasm were excluded. Survival was estimated using Cox proportional-hazards modeling, with age, sex, and specific type of ANLL as covariates. The 6271 patients with de novo ANLL had an estimated 12-month survival of 30%, while the 107 patients with treatment-related ANLL (radiation therapy, 60; chemotherapy, 29; both, 18) had an estimated 12-month survival of 10%. This is not due to lingering effects of the first tumor since ANLL following solid tumors not treated with chemotherapy or radiation therapy (118 cases) has similar survival (estimated 12-month survival, 36%) as de novo ANLL. We conclude that ANLL that occurs after chemotherapy or radiation therapy is biologically more aggressive and/or resistant to therapy than spontaneous ANLL. This provides a rationale for current studies on treatment-induced cellular changes and on more aggressive therapy for these patients.

Aged↗