Biomedical subjects

M Melendez

Publications and source records attributed to M Melendez.

At least 19 recordsLinked to original sources

PubMed2003

Widow and widower remarriage: an analysis in a rural 19th century Costa Rican population and a cross-cultural discussion.

Although the topic of remarriage features saliently in the cultural anthropological literature, it is virtually absent in the biological anthropology journals. This is perplexing, given that remarriage affects the differential reproductive success of males and females in a community, and could well impact a community's population structure. In this paper, we research remarriage practices in a rural 19th century community in Costa Rica. Although we find support for the proposition that males are more likely to remarry than females, we find that widows who remarry are not all young and able to reproduce. Our findings support the cross-culturally-generated suggestion that a female's ability not to remarry is tied to her to ability to own property. Remarriage is a topic of interest to biological anthropologists from a cross-cultural and biocultural perspective.

Age Factors↗

PubMed2001

Sciatic nerve reconstruction: limb preservation after sarcoma resection.

Limb salvage for extremity sarcoma has become the standard of care when possible. This review attempts to determine the outcome of sciatic nerve reconstruction after surgical tumor resection. The authors' objective was to determine the clinical value of extremity salvage with such a defect. Five patients (two male, three female) were selected from a department database at The University of Texas M.D. Anderson Cancer Center between 1995 and 1999 who met the following criteria: lower limb tumor resection involving a gap in the sciatic nerve with subsequent nerve autograft reconstruction. An additional patient who underwent primary sciatic nerve neurorrhaphy was also included. The average tumor size was 203 cm2. The most common tumor histology was spindle cell sarcoma. The average autograft length was 13 +/- 3.2 cm with one to four cables employed. Currently, 3 patients are still alive. Four of the 5 patients who received sciatic autonerve grafts reported partial distal sensory recovery subjectively. The patient who underwent primary neurorrhaphy has both motor and sensory innervation 42 months after surgery. Although not ideal for all patients, sciatic nerve reconstruction is a viable option for those willing to undergo limb preservation. Notable limitations to daily activity do not appear to be present, and patients are able to ambulate with or without assistive devices. With aggressive rehabilitation, some patients are able to function quite well with this bioprosthesis. Patients should consider, however, that their extremity is on loan. Substantial wound complications or infections may ultimately lead to amputation.

Adult↗

PubMed2000

Identification of vaccine candidates for experimental visceral leishmaniasis by immunization with sequential fractions of a cDNA expression library.

Visceral leishmaniasis caused by the intracellular parasite Leishmania donovani is a significant public health problem in many regions of the world. Because of its large genome and complex biology, developing a vaccine for this pathogen has proved to be a challenging task and, to date, protective recombinant vaccine candidates have not been identified. To tackle this difficult problem, we adopted a reductionist approach with the intention of identifying cDNA sequences in an L. donovani amastigote cDNA library that collectively or singly conferred protection against parasite challenge in a murine model of visceral leishmaniasis. We immunized BALB/c mice with plasmid DNA isolated and pooled from 15 cDNA sublibraries ( approximately 2,000 cDNAs/sublibrary). Following systemic challenge with L. donovani, mice immunized with 6 of these 15 sublibraries showed a significantly reduced (35- to 1,000-fold) hepatic parasite burden. Because of the complexity and magnitude of the sequential fractionation-immunization-challenge approach, we restricted our attention to the two sublibraries that conferred the greatest in vivo protection. From one of these two sublibraries, we identified several groups of cDNAs that afforded protection, including a set of nine novel cDNAs and, surprisingly, a group of five cDNAs that encoded L. donovani histone proteins. At each fractionation step, the cDNA sublibraries or the smaller DNA fractions that afforded in vivo protection against the parasite also induced in vitro parasite-specific T helper 1 immune responses. Our studies demonstrate that immunization with sequential fractions of a cDNA library is a powerful strategy for identifying anti-infective vaccine candidates.

Animals↗

PubMed1997

Mechanisms of chlorpheniramine maleate release from hydrophilic swellable polymer systems.

The main objective of this work is to attempt to understand better the mechanism of release of highly water soluble drugs from a swellable polymer and to quantify the amount of drug released. Tablets containing 10% w/w drug, hydroxypropylmethylcellulose E4M (10% w/w, 20% w/w and 30% w/w), 1% w/w magnesium stearate and quantity sufficient to 100% w/w with Lactose Fast Flo as diluent were prepared using the direct compression method. The amount of drug released due to Fickian diffusion and non-Fickian diffusion (polymer relaxation) was quantified at different time intervals. In order to determine if the drug release was Fickian diffusion or non-Fickian diffusion, the exponent n obtained from the equation: Mt/M yen = Ktn was calculated. It was found to be above 0.5 for restricted and unrestricted systems indicating non-Fickian diffusion. Also, the approximate contribution of Fickian diffusion and polymer relaxation to the non-Fickian anomalous release process was calculated. The data obtained from one tablet surface and all surfaces exposed to the dissolution medium demonstrated that Fickian diffusion predominated for the first hour. After one hour of testing dissolution, the relaxational mechanism predominated. The percent drug release from restricted matrices at 6 hours of dissolution testing was 77.9% by polymer relaxation and 27.9% by Fickian diffusion.

Chlorpheniramine↗

PubMed1995

The pathophysiologic relationships between lesion pathology, intracranial ictal EEG onsets, and hippocampal neuron losses in temporal lobe epilepsy.

In temporal lobe epilepsy (TLE) lesion patients the pathology, location of intracranial ictal EEG onsets, and hippocampal neuron losses were compared. Patients (n = 63) were classified into: (1) Tumors (n = 26, e.g. astrocytomas, gangliogliomas); (2) vascular (n = 9, e.g. cavernous and venous angiomas); (3) developmental (n = 17, e.g. cortical dysplasia, heterotopias); or (4) atrophic (n = 11, e.g. cortical or white matter encephalomalacia). Other variables were; (1) the location of the temporal lesion in the mesial to lateral, and anterior to posterior plane, (2) a clinical history of an initial precipitating injury (IPI) prior to the onset of TLE (e.g. prolonged first seizure, head trauma), (3) hippocampal neuron densities, (4) focal or regional location by intracranial depth EEG of ictal onsets, and (5) seizure outcomes. Results showed that severe hippocampal neuron losses were associated with two statistically significant findings. First, patients with mesial lesions in or adjacent to the body of the hippocampus had greater neuron losses compared to mesial lesions anterior or posterior to the hippocampus (P = 0.04). Second, lesion patients with an IPI history had greater Ammon's horn (AH) neuron losses compared to those without IPI histories (P = 0.0005), and the profile of loss was similar to hippocampal sclerosis (HS). Granule cell losses correlated in a complex manner in that; 1) by regression analysis densities decreased with longer intervals of TLE (P = 0.006), (2) tumor patients with IPIs had less granule cell loss compared to those without IPIs intervals of TLE (P = 0.006), (2) tumor patients with IPIs had less granule cell loss compared to those without IPIs (P = 0.05), and (3) developmental patients with IPIs had greater granule cell loss than patients without IPIs (P = 0.009). Mesial-temporal depth EEG electrodes were the first areas of ictal activity in 15 of 16 patients (94%), and greater hippocampal neuron losses were not associated with focal mesial-temporal EEG onsets. Seizure outcomes were worse in tumor patients compared to HS patients (P = 0.01), and patients with post-resection seizures had incomplete resections of their lesions and/or hippocampi. These results indicate that in TLE lesion patients the amount and pattern of hippocampal neuron loss depends on the location of the lesion, the pathologic classification, and a history of an IPI. Further, despite variable neuron losses, in temporal lesion patients the hippocampus was nearly always involved in the genesis or propagation of the chronic seizures.

Case-Control Studies↗

PubMed1995

The clinical-pathogenic mechanisms of hippocampal neuron loss and surgical outcomes in temporal lobe epilepsy.

A retrospective study was carried out to determine whether a prior cerebral injury or medical illness was associated with hippocampal sclerosis in intractable, surgically treated temporal lobe epilepsy (TLE), or whether there was evidence for progressive hippocampal neuron damage from repeated seizures. Temporal lobe epilepsy patients (n = 162) from one epilepsy centre were retrospectively and blindly catalogued into groups based on the presence or absence of an initial precipitating injury (IPI) and whether, when an IPI was present, it had involved seizures (independent variables). Patients were catalogued into four groups: (i) non-seizure IPIs (Group A; n = 54); (ii) IPIs with a prolonged seizure (Group B; n = 66); (iii) IPIs with repetitive non-prolonged seizures (Group C; n = 20); (iv) or no IPIs and idiopathic TLE (Group D; n = 22). The dependent variables were: the differences in the time course of clinical seizures, and quantified hippocampal neuron counts and seizure outcomes. Statistically significant (ANOVA at least P < 0.05) results showed the following. (i) Patients with IPIs (Groups A, B and C) had hippocampal sclerosis, while those with idiopathic TLE (Group D) showed fewer neuron losses and worse post-resection seizure relief. (ii) Patients with non-seizure IPIs (Group A) were on average older at injury; had a longer latent period; showed less neuron losses in Ammon's horn, CA1 and prosubiculum than seizure associated IPIs (Groups B and/or C). (iii) Initial precipitating injury patients with repetitive non-prolonged seizures (Group C) showed the shortest latent period, earliest age of TLE onset, and less CA2 damage than the other IPI groups. Other findings that were statistically significant by analysis of covariance along with the IPI category included the following. (i) CA1 (P = 0.0097) and prosubiculum (P = 0.0089) neuron losses were greater in patients when their TLE was longer than 22 years. (ii) IPIs after age 4 years were associated with latent periods shorter than 10 years compared with variable and longer latent periods of IPIs before age 4 years (P = 0.0015). These results indicate that in surgically treated TLE, hippocampal sclerosis and good seizure outcomes are associated with IPIs. Most of the hippocampal damage found at surgery and the clinical time course of the habitual TLE are influenced by the pathogenic IPI mechanism. However, some secondary neuron losses were associated with longer TLE seizure histories.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗

PubMed1994

Traumatic compared to non-traumatic clinical-pathologic associations in temporal lobe epilepsy.

This study determined differences in clinical-pathologic characteristics of intractable temporal lobe epilepsy (TLE) patients whose mechanism of cerebral injury and chronic seizures involved a prior history of cerebral trauma compared to those with non-traumatic initial injuries. TLE patients (n = 120) from a single epilepsy center were retrospectively and blindly catalogued into pathogenic groups (independent variables) based on if there was a significant Birth injury (n = 11) or Cerebral trauma (n = 26). These two 'trauma' categories were compared to TLE patients with non-seizure non-trauma histories (Non-Sz/Non-Trauma; n = 17), or a first Prolonged seizure (n = 66). The four groups were compared for differences in the time course of their clinical injuries and seizures, quantified hippocampal neuron counts, other temporal neocortical pathologies, and seizure outcomes (dependent variables). Between group statistically significant (at least P < 0.05) results showed: (1) In Birth injury, 33% had Ammon's Horn (AH) neuron loss under 50%, 54% had other temporal neocortical pathologies, they showed the most CA4 neuron loss, and the worse seizure outcomes. (2) Cerebral trauma were older when injured, 29% had AH loss under 50%, 50% showed other pathologies, and they had the best seizure outcomes. (3) Non-Sz/Non-Trauma showed the least AH and CA4 neuron losses, only 12% had other temporal pathologies, and they had seizure outcomes that were intermediate. (4) Prolonged seizure showed the youngest age of habitual TLE onsets, the greatest AH, CA1, and prosubiculum neuron loss, only 11% had other temporal pathologies, and their seizure outcomes were excellent. These results indicate that in intractable surgically treated TLE, a history of cerebral trauma or birth injury as the pathogenic mechanism of their seizures show different clinical-pathologic features and seizure outcomes compared to non-trauma patients. This supports the notion that in TLE there are different pathogenic mechanisms associated with different types of initial injuries and that patients will have different responses to surgical therapy.

Birth Injuries↗

PubMed1987