The administration of therapy for M. tuberculosis infection under direct observation leads to significant reductions in the frequency of primary drug resistance, acquired drug resistance, and relapse.

An abundance of evidence exists that shows calcium channel blockade promotes injury in cultured neurons. However, few studies have addressed the in vivo toxicity of such agents. We now show that the L-type calcium channel antagonist nimodipine promotes widespread and robust injury throughout the neonatal rat brain, in an age-dependent manner. Using both isolated neuronal as well as brain slice approaches, we address mechanisms behind such injury. These expanded studies show a consistent pattern of injury using a variety of agents that lower intracellular calcium. Collectively, these observations indicate that postnatal brain development represents a transitional period for still developing neurons, from being highly sensitive to reductions in intracellular calcium to being less vulnerable to such changes. These observations directly relate to current therapeutic strategies targeting neonatal brain injury.

PIAT was not associated with the duration of delay in tuberculosis diagnosis and treatment and did not significantly change during follow-up. These data demonstrate that, for many individuals, the completion of tuberculosis treatment is the beginning, not the end, of their tuberculosis illness.

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Background-Host pathogen relationships can be classified as allopatric, when the pathogens originated from separate, non-overlapping geographic areas from the host; or sympatric, when host and pathogen shared a common ancestral geographic location. It remains unclear if hostpathogen relationships, as defined by phylogenetic lineage, influence clinical outcome. We sought to examine the association between allopatric and sympatric phylogenetic Mycobacterium tuberculosis lineages and pulmonary impairment after tuberculosis (PIAT).

BackgroundDisparities in outcomes associated with race and ethnicity are well documented for many diseases and patient populations. Tuberculosis (TB) disproportionately affects economically disadvantaged, racial and ethnic minority populations. Pulmonary impairment after tuberculosis (PIAT) contributes heavily to the societal burden of TB. Individual impacts associated with PIAT may vary by race/ethnicity or socioeconomic status.MethodsWe analyzed the pulmonary function of 320 prospectively identified patients with pulmonary tuberculosis who had completed at least 20 weeks standard anti-TB regimes by directly observed therapy. We compared frequency and severity of spirometry-defined PIAT in groups stratified by demographics, pulmonary risk factors, and race/ethnicity, and examined clinical correlates to pulmonary function deficits.ResultsPulmonary impairment after tuberculosis was identified in 71% of non-Hispanic Whites, 58% of non-Hispanic Blacks, 49% of Asians and 32% of Hispanics (p < 0.001). Predictors for PIAT varied between race/ethnicity. PIAT was evenly distributed across all levels of socioeconomic status suggesting that PIAT and socioeconomic status are not related. PIAT and its severity were significantly associated with abnormal chest x-ray, p < 0.0001. There was no association between race/ethnicity and time to beginning TB treatment, p = 0.978.ConclusionsDespite controlling for cigarette smoking, socioeconomic status and time to beginning TB treatment, non-Hispanic White race/ethnicity remained an independent predictor for disproportionately frequent and severe pulmonary impairment after tuberculosis relative to other race/ethnic groups. Since race/ethnicity was self reported and that race is not a biological construct: these findings must be interpreted with caution. However, because race/ethnicity is a proxy for several other unmeasured host, pathogen or environment factors that may contribute to disparate health outcomes, these results are meant to suggest hypotheses for further research.

The complaint of chronic fatigue is ubiquitous in the primary care setting. Because of the nonspecific nature of chronic fatigue, practitioners do not focus on this complaint. Furthermore, most physicians use a problem-based approach. Such a prematurely narrowed focus could overlook the chronic fatigue complaint. Omissions in the data collection process would prove this oversight. Therefore, we postulated that a retrospective review of evaluations for chronic fatigue would demonstrate significant categorical deficiencies. These deficiencies would indicate a problem focus different than the chronic fatigue complaint itself. The authors reviewed the current literature to establish historical, physical, and laboratory findings pertinent to the evaluation of chronic fatigue. Six major categories and the associated data elements were identified for use in analyzing patient records. The patient records from the preceding 6 months were reviewed to find those containing a complaint of chronic fatigue. These records were analyzed to determine if a complete data set had been sought and if an associated diagnosis was made. A total of 425 consecutive charts from an academic family practice clinic were retrospectively reviewed; 9.9% (42) mentioned chronic fatigue. Physicians were lax in performing the mental status and physical examinations; taking the patient's psychiatric and sleep history, as well as the history of chief complaint; and ordering laboratory evaluations. The physician diagnoses included: depression (40.4%), nonspecific fatigue (35.7%), general medical disorders (16.6%), chronic fatigue syndrome (2.4%), fibromyalgia (2.4%), and sleep apnea (2.4%). From these data, the investigators conclude that the workup for chronic fatigue is often incomplete or lacks documentation. This oversight is likely due to a problem focus not directed at the chronic fatigue complaint. Also complicating the evaluation process are the multiple associated disorders, the prevalence of the complaint, and costibenefit issues facing the primary care physician.

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