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Objectives: Investigate the use of nasal endoscopy, sinus imaging, and neurologic evaluation in patients presenting to a rhinologist primarily for craniofacial pain.Methods: This was a retrospective analysis of consecutive outpatients presenting to a rhinologist between 2016 and 2019 with chief complaints of craniofacial pain with or without other sinonasal symptoms, who were then referred to and evaluated by headache specialists. Data analyzed included sinusitis symptoms, Sino-Nasal Outcome Test (SNOT-22) scores (and facial pain subscores), pain location, nasal endoscopy, computed tomography (CT) findings, and headache diagnoses made by headache specialists.Results: Of the 134 patients with prominent craniofacial pain, the majority of patients were diagnosed with migraine (50%) or tension-type (22%) headache, followed by multiple other non-sinogenic headache disorders. Approximately 5% of patients had headaches attributed to sinusitis. Amongst all patients, 90% had negative nasal endoscopies. Patients with negative endoscopies were significantly less likely to report smell loss (P= .003) compared to those with positive endoscopies. Poor agreement was demonstrated between self-reported pain locations and sinus findings on CT (kappa values < 0.20). Negative nasal endoscopy showed high concurrence with negative CT findings (80%-97%).Conclusions: Patients presenting with chief complaints of craniofacial pain generally met criteria for various non-sinogenic headache disorders. Nasal endoscopy was negative in 90% of patients, and CT demonstrated poor agreement with pain locations. Nasal endoscopy and CT shared high concurrence rates for negative sinus findings. The value of nasal endoscopy over sinus imaging in craniofacial pain evaluation should be explored in future studies.

Background Orbital, intracranial, and osseous extra-sinus complications can arise from bacterial or fungal sinusitis. Odontogenic sinusitis (ODS) can cause extra-sinus complications, but its prevalence remains poorly characterized.Objective To determine the frequency of ODS as a cause of operative extra-sinus infectious complications and describe clinical features of all complicated sinusitis cases.Methods A multi-institutional retrospective review was performed on all operative sinusitis-related extra-sinus complications from 2011 to 2020. ODS was diagnosed by sinus computed tomography (CT) and dental evaluations when available. Demographics, complication types, sinusitis etiologies, and various clinical features were analyzed.Results Forty-five patients were included (mean age 55.5 years, 56% male). Of the extra-sinus complications, 40% were orbital only, 22% intracranial only, 13% osseous only, and 25% involved combined complications. The 2 most common causes of extra-sinus complications were ODS (40%) and mucopyocele (27%). When invasive fungal etiologies were excluded, and only unilateral maxillary opacification on CT was considered, nearly 60% of extra-sinus complications were due to ODS. Unilateral maxillary sinus opacification on CT was present in 100% of complicated ODS compared to 44% of nonodontogenic cases, and oral anaerobes were only identified in ODS cases. No complicated ODS patients underwent dental interventions during hospitalization.Conclusion ODS was the most common cause of operative extra-sinus infectious complications. Clinicians should consider ODS high on the differential diagnosis of all patients presenting with complicated sinusitis, especially when sinusitis is unilateral and invasive fungal infection is not suspected.

Background: Children with heightened airway responsiveness have a greater tendency to develop asthma symptoms. Many existing studies describing this relationship have relied on self-reported symptoms that may be prone to [...]

Objective: The authors' goal was to construct a short screening scale for DSM-IV posttraumatic stress disorder (PTSD). Method: They used data from the Detroit Area Survey of Trauma, which is a representative population sample of 2,181 subjects 18-45 years of age. Random digit dialing was used to select the sample, and a computer-assisted telephone interview was used to collect data on traumatic experiences and PTSD. Presence or absence of PTSD was assessed with a telephone-administered structured interview that closely followed the National Institute of Mental Health Diagnostic Interview Schedule for DSM-IV and the World Health Organization Composite International Diagnostic Interview, version 2.1. Best-subset regression analysis and receiver operating characteristic analysis were used to select a subset of items from the structured interview that most efficiently predicted PTSD as diagnosed in the full-length interview. Results: A seven-symptom screening scale for PTSD was selected; five of the symptoms were from the avoidance and numbing group, and two were from the hyperarousal group. A score of 4 or greater on this scale defined positive cases of PTSD with a sensitivity of 80%, specificity of 97%, positive predictive value of 71%, and negative predictive value of 98%. Conclusions: The short screening scale is an efficient method to screen for PTSD in epidemiologic and clinical studies, given limitations on resources and burden on respondents.

Objective: To test for a suspected adverse effect of low birth weight ([less than or equal to] 2500 g) on IQ at age 6 years in two socioeconomically disparate populations. Design: Nonconcurrent prospective study. Setting: An urban, predominantly disadvantaged population and a suburban middle-class population in southeastern Michigan. Participants: Low-birth-weight (N=473) and normal-birth-weight (N=350) subjects, randomly selected from the 1983 through the 1985 newborn lists of two major hospitals, one serving an urban and the other a suburban population. Main Outcome Measure: The Wechsler Intelligence Scale for Children-Revised to measure IQ. Results: The mean full-scale IQ of low-birth-weight children was 4.9 points lower than that of normal-birth-weight children, controlling for population site, maternal IQ, maternal education, and race (95% confidence interval [CI] 3.0 to 6.8). There was no evidence of low-birth-weight interaction with population site, and the same IQ difference was detected in both populations. In the urban population, low birth weight was associated with an increased risk for IQ below 85 (odds ratio, 2.2; 95% CI, 1.3 to 3.7). In the suburban population, low birth weight was associated with an increased risk for IQ below 100 (odds ratio, 2.0; 95% CI, 1.2 to 3.4). A gradient relationship with full-scale IQ was observed, with the largest deficit in those born weighing 1500 g or less, an intermediate deficit in those born weighing 1501 through 2000 g, and the least pronounced deficit in those born weighing 2001 through 2500 g. Conclusions: The overall effect of low birth weight represents an increase of approximately 10% of low-birth-weight children with an IQ of more than 1 SD below the population's mean. Children born weighing 2000 g or less bore the major burden of the IQ deficits. (Arch Pediatr Adolesc Med. 1994;148:377-383), Low birth weight (LBW) appears to reduce the IQ in a pattern related to how low the birth weight is. IQ was measured at age six in 473 children with birth weights less than or equal to 2500 g who were free of neurologic impairment. One group was born at a hospital serving suburban middle-class Detroit children and the other was born at a hospital serving Detroit inner-city children. To minimize the effect of confounding social variables, outcomes for each group were compared with that of 350 normal-birth-weight (over 2500 g) children born at the same hospitals. The average IQ was reduced by 4.9 points after controlling for site, maternal IQ, maternal education and race. The deficit was the same at both sites. This meant that 10% more LBW children had IQs below the threshold that defines clinical concern. When the group was stratified by birth weight, the largest deficit was among children weighing less than 1500 g, the next largest among children weighing 1501 through 2000 g, and the smallest among children weighing over 2000 g.

The objective of this study was to assess the utility of bioelectrical impedance analysis (BIA) in determining nutritional status in critically ill patients in the intensive care unit (ICU). Data were collected prospectively in 33 mechanically ventilated medical and surgical ICU patients requiring nutrition as part of their care. BIA, with subsequent calculation of body-composition indexes, was performed every other day for the duration of ICU stay. Body cell mass (BCM) changes correlated with energy and protein intakes ([r.sup.2] = 0.87, P < 0.001 and [r.sup.2] = 0.67, P < 0.001, respectively). Maintenance of BCM was achieved by a daily provision of 125.5 kJ . [kg.sup.-1] [.d.sup.-1] (30 kcal . [kg.sup.-1] [.d.sup.-1]) and 1.5 g protein/kg whereas greater intakes allowed restoration of BCM. The mean ratios of exchangeable sodium to potassium ([Na.sub.e]:[K.sub.e]) improved only in patients achieving positive nitrogen balance (P = 0.013). Body-composition changes determined by BIA represent a feasible adjunctive method for evaluating and monitoring nutritional status in ICU patients.

The policies of insurance carriers have used the truncal vein size as a criterion for coverage. The objective of the present study was to compare the effect of great saphenous vein (GSV) size ≥5 mm vs <5 mm on patient presentation and clinical outcomes.

To improve enrollment and participation in cardiac rehabilitation (CR), alternate models such as hybrid-CR (combined clinic- and telehealth home-based) need to be implemented. This study showed that the telehealth-CR sessions used for hybrid-CR result in exercise training intensities that were not significantly different from standard facilitybased CR.

Risk factors for pulmonary embolism in patients with coronavirus disease 2019 include obesity, an elevated d-dimer value, elevated C-reactive protein level, and a rising d-dimer value over time.

Background When chronic rhinosinusitis with nasal polyps (CRSwNP) fails to respond to medical therapy, endoscopic sinus surgery (ESS) plays an integral role in management. Some studies have shown that middle turbinate resection (MTR) during ESS leads to decreased polyp recurrence and revision ESS rates. Other studies suggest MTR can lead to complications.Objective The purpose of this study was to assess the safety of MTR during ESS for CRSwNP by determining the incidences of intraoperative cerebrospinal fluid (CSF) leak, postoperative epistaxis requiring operative intervention, and postoperative complete frontal stenosis.Methods A multiinstitutional, prospective case series of 91 adult CRSwNP patients was conducted. Patients with medically refractory CRSwNP underwent primary or revision ESS plus MTR by 3 surgeons. Two of the surgeons performed partial MTRs, and one of the surgeons performed complete MTRs. Patients were evaluated for the following complications: intraoperative CSF leak during MTR, postoperative epistaxis requiring operative intervention, and postoperative complete frontal ostial stenosis. Secondary outcomes included changes from preoperative to postoperative 22-item Sinonasal Outcome Test (SNOT-22) scores and revision ESS rates.Results Unilateral or bilateral complete ESSs with MTRs were performed on 91 CRSwNP patients. In total, 173 MTRs were performed. Two surgeons performed 97 partial MTRs on 49 patients, and the third surgeon performed 76 complete MTRs on 42 patients. One CSF leak occurred during partial MTR (1/173, 0.57%). No patients suffered postoperative epistaxis requiring operative intervention, and no patients developed complete frontal stenosis. From preoperatively to postoperatively, mean SNOT-22 scores decreased from 53.7 to 13.1 (P= .001). No revision ESS was needed during the follow-up period. Mean follow-up time was 7.5 ± 5.4 months.Conclusions Partial and complete MTR during ESS for CRSwNP in this cohort resulted in very low, acceptable intraoperative and short-term postoperative complication rates and no detriment to SNOT-22 scores.

The antifibrotic peptide N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is released from thymosin-β4 (Tβ4) by the meprin-α and prolyl oligopeptidase (POP) enzymes and is hydrolyzed by angiotensin-converting enzyme (ACE). Ac-SDKP is present in urine; however, it is not clear whether de novo tubular release occurs or if glomerular filtration is the main source. We hypothesized that Ac-SDKP is released into the lumen of the nephrons and that it exerts an antifibrotic effect. We determined the presence of Tβ4, meprin-α, and POP in the kidneys of Sprague-Dawley rats. The stop-flow technique was used to evaluate Ac-SDKP formation in different nephron segments. Finally, we decreased Ac-SDKP formation by inhibiting the POP enzyme and evaluated the long-term effect in renal fibrosis. The Tβ4 precursor and the releasing enzymes meprin-α and POP were expressed in the kidneys. POP enzyme activity was almost double that in the renal medulla compared with the renal cortex. With the use of the stop-flow technique, we detected the highest Ac-SDKP concentrations in the distal nephron. The infusion of a POP inhibitor into the kidney decreased the amount of Ac-SDKP in distal nephron segments and in the proximal nephron to a minor extent. An ACE inhibitor increased the Ac-SDKP content in all nephron segments, but the increase was highest in the distal portion. The chronic infusion of a POP inhibitor increased kidney medullary fibrosis, which was prevented by Ac-SDKP. We conclude that Ac-SDKP is released by the nephron and is part of an important antifibrotic system in the kidney.

Zucker obese rats (ZOR) have higher glomerular capillary pressure (PGC) that can cause renal damage. PGCis controlled by afferent (Af-Art) and efferent arteriole (Ef-Art) resistance. Af-Art resistance is regulated by factors that regulate other arterioles, such as myogenic response. In addition, it is also regulated by 2 intrinsic feedback mechanisms: 1) tubuloglomerular feedback (TGF) that causes Af-Art constriction in response to increased NaCl in the macula densa and 2) connecting tubule glomerular feedback (CTGF) that causes Af-Art dilatation in response to an increase in NaCl transport in the connecting tubule via the epithelial sodium channel. Since CTGF is an Af-Art dilatory mechanism, we hypothesized that increased CTGF contributes to TGF attenuation, which in turn increases PGCin ZOR. We performed a renal micropuncture experiment and measured stop-flow pressure (PSF), which is an indirect measurement of PGCin ZOR. Maximal TGF response at 40 nl/min was attenuated in ZOR (4.47 ± 0.60 mmHg) in comparison to the Zucker lean rats (ZLR; 8.54 ± 0.73 mmHg, P< 0.05), and CTGF was elevated in ZOR (5.34 ± 0.87 mmHg) compared with ZLR (1.12 ± 1.28 mmHg, P< 0.05). CTGF inhibition with epithelial sodium channel blocker normalized the maximum PSFchange in ZOR indicating that CTGF plays a significant role in TGF attenuation (ZOR, 10.67 ± 1.07 mmHg vs. ZLR, 9.5 ± 1.53 mmHg). We conclude that enhanced CTGF contributes to TGF attenuation in ZOR and potentially contribute to progressive renal damage.

Objective: To learn whether cigarette smoking by persons other than parents significantly contributes to the passive environmental tobacco smoke (ETS) exposure of infants. Study Design: A cohort of infants prospectively followed up from birth to age 2 years with monthly questionnaires concerning smoking by different categories of adults coming into contact with the infants. Setting: Health maintenance organization members residing in several suburban communities of Detroit, Mich, defined by contiguous ZIP codes. Subjects: Ninety-seven (83%) of 117 healthy, full-term infants, thought to be at high risk of allergic disease based on cord blood IgE, who were born to eligible mothers and who completed 24 months of follow-up. Main Outcome Measures: Average of bimonthly urinary cotinine-creatinine ratios (CCRs) during the 2 years of the study. Results: There were significant correlations (r [is less than or equal to] 0.28, P [is less than or equal to] .005) between the frequency of smoking by all 7 categories of adults considered and the average CCRs of the infants. Multivariable analysis demonstrated that average urinary CCRs were significantly associated not only with smoking by the infant's parents, but also with smoking by workers at day care away from the home, persons visited away from the home, and persons other than parents residing in the home (overall [R.sup.2]=0.72, P=.001). Conclusions: Smoking by multiple individuals, other than the parents, significantly contributes to the ETS exposure of infants. These findings suggest that, at least for infants, efforts to reduce the adverse health effects of ETS exposure should extend beyond curtailing parental smoking. Arch Pediatr Adolesc Med. 2000;154:1237-1241

Background: Asthma morbidity and mortality are higher in the United States for African-American (AA) children when compared to European-American (EA) children. Study objectives: To explore racial differences in physiologic factors [...]

Unilaterally nephrectomized rats (UNx) have higher glomerular capillary pressure (PGC) that can cause significant glomerular injury in the remnant kidney. PGCis controlled by the ratio of afferent (Af-Art) and efferent arteriole resistance. Af-Art resistance in turn is regulated by two intrinsic feedback mechanisms: 1) tubuloglomerular feedback (TGF) that causes Af-Art constriction in response to increased NaCl in the macula densa; and 2) connecting tubule glomerular feedback (CTGF) that causes Af-Art dilatation in response to an increase in NaCl transport in the connecting tubule via the epithelial sodium channel (ENaC). Resetting of TGF post-UNx can allow systemic pressure to be transmitted to the glomerulus and cause renal damage, but the mechanism behind this resetting is unclear. Since CTGF is an Af-Art dilatory mechanism, we hypothesized that CTGF is increased after UNx and contributes to TGF resetting. To test this hypothesis, we performed UNx in Sprague-Dawley (8) rats. Twenty-four hours after surgery, we performed micropuncture of individual nephrons and measured stop-flow pressure (PSF). PSFis an indirect measurement of PGC. Maximal TGF response at 40 nl/min was 8.9 ± 1.24 mmHg in sham-UNx rats and 1.39 ± 1.02 mmHg in UNx rats, indicating TGF resetting after UNx. When CTGF was inhibited with the ENaC blocker benzamil (1 μM/l), the TGF response was 12.29 ± 2.01 mmHg in UNx rats and 13.03 ± 1.25 mmHg in sham-UNx rats, indicating restoration of the TGF responses in UNx. We conclude that enhanced CTGF contributes to TGF resetting after UNx.

Renal blood flow (RBF) provides important information regarding renal physiology and nephropathies. Arterial spin labeling–magnetic resonance imaging (ASL-MRI) is a noninvasive method of measuring blood flow without exogenous contrast media. However, low signal-to-noise ratio and respiratory motion artifacts are challenges for RBF measurements in small animals. Our objective was to evaluate the feasibility and reproducibility of RBF measurements by ASL-MRI using respiratory-gating and navigator correction methods to reduce motion artifacts. ASL-MRI images were obtained from the kidneys of Sprague-Dawley (SD) rats on a 7-Tesla Varian MRI system with a spin-echo imaging sequence. After 4 days, the study was repeated to evaluate its reproducibility. RBF was also measured in animals under unilateral nephrectomy and in renal artery stenosis (RST) to evaluate the sensitivity in high and low RBF models, respectively. RBF was also evaluated in Dahl salt-sensitive (SS) rats and spontaneous hypertensive rats (SHR). In SD rats, the cortical RBFs (cRBF) were 305 ± 59 and 271.8 ± 39 ml·min−1·100 g tissue−1in the right and left kidneys, respectively. Retest analysis revealed no differences (P= 0.2). The test-retest reliability coefficient was 92 ± 5%. The cRBFs before and after the nephrectomy were 296.8 ± 30 and 428.2 ± 45 ml·min−1·100 g tissue−1(P= 0.02), respectively. The kidneys with RST exhibited a cRBF decrease compared with sham animals (86 ± 17.6 vs. 198 ± 33.7 ml·min−1·100 g tissue−1; P< 0.01). The cRBFs in SD, Dahl-SS, and SHR rats were not different (P= 0.35). We conclude that ASL-MRI performed with navigator correction and respiratory gating is a feasible and reliable noninvasive method for measuring RBF in rats.

Patients diagnosed with skin conditions have a higher risk of comorbid psychiatric conditions and suicide-related outcomes such as suicidal ideations and behaviors. There is paucity of evidence in the US general population about the risk of suicide death in patients with dermatologic conditions.

Afferent arteriole (Af-Art) resistance is modulated by two intrinsic nephron feedbacks: 1) the vasoconstrictor tubuloglomerular feedback (TGF) mediated by Na+-K+-2Cl−cotransporters (NKCC2) in the macula densa and blocked by furosemide and 2) the vasodilator connecting tubule glomerular feedback (CTGF), mediated by epithelial Na+channels (ENaC) in the connecting tubule and blocked by benzamil. High salt intake reduces Af-Art vasoconstrictor ability in Dahl salt-sensitive rats (Dahl SS). Previously, we measured CTGF indirectly, by differences between TGF responses with and without CTGF inhibition. We recently developed a new method to measure CTGF more directly by simultaneously inhibiting NKCC2 and the Na+/H+exchanger (NHE). We hypothesize that in vivo during simultaneous inhibition of NKCC2 and NHE, CTGF causes an Af-Art dilatation revealed by an increase in stop-flow pressure (PSF) in Dahl SS and that is enhanced with a high salt intake. In the presence of furosemide alone, increasing nephron perfusion did not change the PSFin either Dahl salt-resistant rats (Dahl SR) or Dahl SS. When furosemide and an NHE inhibitor, dimethylamiloride, were perfused simultaneously, an increase in tubular flow caused Af-Art dilatation that was demonstrated by an increase in PSF.This increase was greater in Dahl SS [4.5 ± 0.4 (SE) mmHg] than in Dahl SR (2.5 ± 0.3 mmHg; P< 0.01). We confirmed that CTGF causes this vasodilation, since benzamil completely blocked this effect. However, a high salt intake did not augment the Af-Art dilatation. We conclude that during simultaneous inhibition of NKCC2 and NHE in the nephron, CTGF induces Af-Art dilatation and a high salt intake failed to enhance this effect.

To the Editor: We read with interest the article in CHEST by Celed6n et al (January 2004) (1) on ethnicity and skin test reactivity to aeroallergens. The authors found that [...]

Connecting tubule glomerular feedback (CTGF) is a mechanism where an increase in sodium (Na) concentration in the connecting tubule (CNT) causes the afferent arteriole (Af-Art) to dilate. We recently reported that aldosterone within the CNT lumen enhances CTGF via a nongenomic effect involving GPR30 receptors and sodium/hydrogen exchanger (NHE), but the signaling pathways of this mechanism are unknown. We hypothesize that aldosterone enhances CTGF via cAMP/protein kinase A (PKA) pathway that activates protein kinase C (PKC) and stimulates superoxide (O2−) production. Rabbit Af-Arts and their adherent CNTs were microdissected and simultaneously perfused. Two consecutive CTGF curves were elicited by increasing the CNT luminal NaCl. We found that the main effect of aldosterone was to sensitize CTGF and we analyzed data by comparing NaCl concentration in the CNT perfusate needed to achieve half of the maximal response (EC50). During the control period, the NaCl concentration that elicited a half-maximal response (EC50) was 37.0 ± 2.0 mmol/l; addition of aldosterone (10−8mol/l) to the CNT lumen decreased EC50to 19.3 ± 1.3 mmol/l (P≤ 0.001 vs. Control). The specific adenylyl cyclase inhibitor 2′,3′-dideoxyadenosine (ddA; 2 × 10−4mol/l) and the PKA inhibitor H-89 dihydrochloride hydrate (H-89; 2 × 10−6mol/l) prevented the aldosterone effect. The selective PKC inhibitor GF109203X (10−8mol/l) also prevented EC50reduction caused by aldosterone. CNT intraluminal addition of O2−scavenger tempol (10−4mol/l) blocked the aldosterone effect. We conclude that aldosterone inside the CNT lumen enhances CTGF via a cAMP/PKA/PKC pathway and stimulates O2−generation and this process may contribute to renal damage by increasing glomerular capillary pressure.

N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a natural tetrapeptide with anti-inflammatory and antifibrotic properties. Previously, we have shown that prolyl oligopeptidase (POP) is involved in the Ac-SDKP release from thymosin-β4 (Tβ4). However, POP can only hydrolyze peptides shorter than 30 amino acids, and Tβ4 is 43 amino acids long. This indicates that before POP hydrolysis takes place, Tβ4 is hydrolyzed by another peptidase that releases NH2-terminal intermediate peptide(s) with fewer than 30 amino acids. Our peptidase database search pointed out meprin-α metalloprotease as a potential candidate. Therefore, we hypothesized that, prior to POP hydrolysis, Tβ4 is hydrolyzed by meprin-α. In vitro, we found that the incubation of Tβ4 with both meprin-α and POP released Ac-SDKP, whereas no Ac-SDKP was released when Tβ4 was incubated with either meprin-α or POP alone. Incubation of Tβ4 with rat kidney homogenates significantly released Ac-SDKP, which was blocked by the meprin-α inhibitor actinonin. In addition, kidneys from meprin-α knockout (KO) mice showed significantly lower basal Ac-SDKP amount, compared with wild-type mice. Kidney homogenates from meprin-α KO mice failed to release Ac-SDKP from Tβ4. In vivo, we observed that rats treated with the ACE inhibitor captopril increased plasma concentrations of Ac-SDKP, which was inhibited by the coadministration of actinonin (vehicle, 3.1 ± 0.2 nmol/l; captopril, 15.1 ± 0.7 nmol/l; captopril + actinonin, 6.1 ± 0.3 nmol/l; P< 0.005). Similar results were obtained with urinary Ac-SDKP after actinonin treatment. We conclude that release of Ac-SDKP from Tβ4 is mediated by successive hydrolysis involving meprin-α and POP.

Hypertension is associated with cardiovascular disease, stroke, and a range of other medical sequelae. Accurate blood pressure (BP) readings, which depend on the integrity and calibration of the measuring device, are essential to identifying suboptimal BP. This study describes calibration rates of aneroid BP devices (a) utilized in home healthcare (HHC) and (b) having the needle resting within the zero accuracy indicator. BP devices from one branch of a home care agency were inspected and checked for calibration according to the protocol set forth by the European Society of Hypertension. Of the 125 devices measured, 78.4% were in calibration. Of the 94 devices with the gauge needle resting in the zero accuracy indicator, 11.7% were not in calibration; whereas, 51.6% of the 31 devices with the gauge needle resting outside the zero accuracy indicator were found not in calibration. Twenty-one devices were not checked for calibration due to inflation bulb malfunction, tubing tears, or excessive wear. Furthermore, visual inspection of the needle placement did not confirm a device as being in or out of calibration. Proper maintenance and routine calibration of BP equipment is foundational to assuring accuracy of BP readings obtained by HHC providers.

Background:Characteristic features of hypokinetic dysarthria develop in Parkinson disease (PD). We hypothesized that quantified acoustic changes of voice might provide a correlate of disease severity.Objective:To determine if there are significant differences in acoustic measures of voice between mild and moderate PD; 2) To evaluate correlations between acoustic parameters of voice and subtests of the UPDRS in mild and moderate PD.Methods:Twenty six participants with PD underwent vocal acoustic testing while off PD medication, for comparison to 22 healthy controls. Participants with PD were divided into two groups based upon UPDRS activities of daily living (ADL) ratings: summed scores were used to define mild and moderate PD. Participants voiced /i/ (“ee”) at comfort, high, and low pitch (3 trials/pitch). The CSpeech Waveform Analysis Program was used to analyze cycle-to-cycle frequency (“jitter”) and amplitude (“shimmer”) irregularities of the vocal signal, signal-to-noise ratio, and maximum phonation frequency range converted to semitones. Sections of UPDRS scores were correlated to acoustic variables of voice.Results:Key findings included a significant difference between the semitone range of the control subjects and the moderate PD group (p = 0.036). Further analyses revealed significant differences in semitone range for males between the controls vs. mild PD (p = 0.014), and controls vs. moderate PD (p = 0.005). Significant correlations were also found between acoustic findings and both the ADL and motor portions of the UPDRS.Conclusions:Acoustic analysis of voice, particularly frequency range, may provide a quantifiable correlate of diseaseprogression in PD.

Systemic lupus erythematosus is an autoimmune disease characterized by the development of auto antibodies against a variety of self-antigens and deposition of immune complexes that lead to inflammation, fibrosis, and end-organ damage. Up to 60% of lupus patients develop nephritis and renal dysfunction leading to kidney failure. N-acetyl-seryl-aspartyl-lysyl-proline, i.e., Ac-SDKP, is a natural tetrapeptide that in hypertension prevents inflammation and fibrosis in heart, kidney, and vasculature. In experimental autoimmune myocarditis, Ac-SDKP prevents cardiac dysfunction by decreasing innate and adaptive immunity. It has also been reported that Ac-SDKP ameliorates lupus nephritis in mice. We hypothesize that Ac-SDKP prevents lupus nephritis in mice by decreasing complement C5-9, proinflammatory cytokines, and immune cell infiltration. Lupus mice treated with Ac-SDKP for 20 wk had significantly lower renal levels of macrophage and T cell infiltration and proinflammatory chemokine/cytokines. In addition, our data demonstrate for the first time that in lupus mouse Ac-SDKP prevented the increase in complement C5-9, RANTES, MCP-5, and ICAM-1 kidney expression and it prevented the decline of glomerular filtration rate. Ac-SDKP-treated lupus mice had a significant improvement in renal function and lower levels of glomerular damage. Ac-SDKP had no effect on the production of autoantibodies. The protective Ac-SDKP effect is most likely achieved by targeting the expression of proinflammatory chemokines/cytokines, ICAM-1, and immune cell infiltration in the kidney, either directly or via C5-9 proinflammatory arm of complement system.

Afferent (Af-Art) and efferent arterioles resistance regulate glomerular capillary pressure. The nephron regulates Af-Art resistance via: 1) vasoconstrictor tubuloglomerular feedback (TGF), initiated in the macula densa via Na-K-2Cl cotransporters (NKCC2) and 2) vasodilator connecting tubuloglomerular feedback (CTGF), initiated in connecting tubules via epithelial Na channels (ENaC). Furosemide inhibits NKCC2 and TGF. Benzamil inhibits ENaC and CTGF. In vitro, CTGF dilates preconstricted Af-Arts. In vivo, benzamil decreases stop-flow pressure (PSF), suggesting that CTGF antagonizes TGF; however, even when TGF is blocked, CTGF does not increase PSF, suggesting there is another mechanism antagonizing CTGF. We hypothesize that in addition to NKCC2, activation of Na/H exchanger (NHE) antagonizes CTGF, and when both are blocked CTGF dilates Af-Arts and this effect is blocked by a CTGF inhibitor benzamil. Using micropuncture, we studied the effects of transport inhibitors on TGF responses by measuring PSFwhile increasing nephron perfusion from 0 to 40 nl/min. Control TGF response (−7.9 ± 0.2 mmHg) was blocked by furosemide (−0.4 ± 0.2 mmHg; P< 0.001). Benzamil restored TGF in the presence of furosemide (furosemide: −0.2 ± 0.1 vs. furosemide+benzamil: −4.3 ± 0.3 mmHg; P< 0.001). With furosemide and NHE inhibitor, dimethylamiloride (DMA), increase in tubular flow increased PSF(furosemide+DMA: 2.7 ± 0.5 mmHg, n= 6), and benzamil blocked this (furosemide+DMA+benzamil: −1.1 ± 0.2 mmHg; P< 0.01, n= 6). We conclude that NHE in the nephron decreases PSF(Af-Art constriction) when NKCC2 and ENaC are inhibited, suggesting that in the absence of NKCC2, NHE causes a TGF response and that CTGF dilates the Af-Art when TGF is blocked with NKCC2 and NHE inhibitors.

The prevalence of medication use among Americans is reported at 48% with significant linear increases with advancing age. A link between specific medication use and fall risk has been established. The purposes of this study are to describe (a) medication categories and (b) medication prevalence associated with fall risk prescribed to individuals case-managed by physical therapists (PTs) in home healthcare (HHC). Descriptive retrospective chart reviews of age, gender, ethnicity, diagnosis, and prescribed medication profiles were obtained from electronic health records (EHRs) of individuals case-managed by PTs at one HHC agency. Descriptive statistics of patient characteristics and medications were analyzed. The chi-square test compared difference by age, gender, and ethnicity. Ninety-five EHRs met criteria for inclusion. Eight hundred and nineteen total medications, comprising 403 medications and 34 medication categories were identified. The highest medication categories prescribed were pain relief(70.5%); cardiovascular agents(65.3%); vitamins, minerals, therapeutic nutrients, and electrolytes(60.0%); gastrointestinal(53.7%); and heart andcholesterolagents(45.3%). Fall risk indicators were identified including medication from a fall risk category (4.2%) and polypharmacy (90.5%). Individuals case-managed by PTs in the HHC setting are prescribed medications from a variety of medication categories including fall risk indicators. This study emphasizes the importance of PTs' review of medications during an initial examination to identify potential adverse events, including falls, which may occur as a result of medication usage.

Inflammation has been proposed as a key component in the development of hypertension and cardiac remodeling associated with different cardiovascular diseases. However, the role of the proinflammatory cytokine interleukin-6 in the chronic stage of hypertension is not well defined. Here, we tested the hypothesis that deletion of interleukin-6 protects against the development of hypertension, cardiac inflammation, fibrosis, remodeling and dysfunction induced by high salt diet and angiotensin II (Ang II).

The afferent arteriole (Af-Art) controls glomerular capillary pressure, an important determinant of glomerular injury. Af-Art myogenic response is mediated by ATP, and ATP signaling is in turn mediated by 20-HETE. Dahl salt-sensitive rats (Dahl SS) have decreased renal 20-HETE production. We hypothesized that Dahl SS have an impaired myogenic response and constrictor response to ATP, due to decreased 20-HETE. Af-Arts from Dahl SS or Dahl salt-resistant rats (Dahl SR) were microdissected and perfused. When myogenic response was induced by increasing Af-Art perfusion pressure from 60 to 140 mmHg, luminal Af-Art diameter decreased in Dahl SR but not in Dahl SS (−3.1 ± 0.8 vs. 0.5 ± 0.8 μm, P< 0.01). The 20-HETE antagonist 20-HEDE (10−6M) blocked the myogenic response in Dahl SR but had no effect in Dahl SS. Addition of a subconstrictor concentration of 20-HETE (but not a subconstrictor concentration of norepinephrine) restored the myogenic response in Dahl SS. We then perfused Af-Arts at 60 mmHg and tested the effects of the ATP analog α,β-methylene-ATP (10−6M). Maximum ATP-induced constriction was attenuated in Dahl SS compared with Dahl SR (1.5 ± 0.5 vs. 7.4 ± 0.8 μm, P< 0.001). 20-HEDE attenuated ATP-induced Af-Art constriction in Dahl SR but not in Dahl SS, and consequently, ATP-induced constriction was no longer different between strains. In conclusion, Dahl SS have an impaired myogenic response and ATP-induced Af-Art constriction due to a decrease in Af-Art 20-HETE. The impaired myogenic responses may contribute to the nephrosclerosis that develops in Dahl SS.

Increasing Na delivery to epithelial Na channels (ENaC) in the connecting tubule (CNT) dilates the afferent arteriole (Af-Art), a process we call connecting tubule glomerular feedback (CTGF). We hypothesize that aldosterone sensitizes CTGF via a nongenomic mechanism that stimulates CNT ENaC via the aldosterone receptor GPR30. Rabbit Af-Arts and their adherent CNTs were microdissected and simultaneously perfused. Two consecutive CTGF curves were elicited by increasing luminal NaCl in the CNT. During the control period, the concentration of NaCl that elicited a half-maximal response (EC50) was 37.0 ± 2.0 mmol/l; addition of aldosterone 10−8mol/l to the CNT lumen caused a left-shift (decrease) in EC50to 19.3 ± 1.3 mmol/l (P= 0.001 vs. control; n= 6). Neither the transcription inhibitor actinomycin D nor the translation inhibitor cycloheximide prevented the effect of aldosterone (control EC50= 34.7 ± 1.9 mmol/l; aldosterone+actinomycin D EC50= 22.6 ± 1.6 mmol/l; P< 0.001 and control EC50= 32.4 ± 4.3 mmol/l; aldosterone+cycloheximide EC50= 17.4 ± 3.3 mmol/l; P< 0.001). The aldosterone antagonist eplerenone prevented the sensitization of CTGF by aldosterone (control EC50= 33.2 ± 1.7 mmol/l; aldosterone+eplerenone EC50= 33.5 ± 1.3 mmol/l; n= 7). The GPR30 receptor blocker G-36 blocked the sensitization of CTGF by aldosterone (aldosterone EC50= 16.5 ± 1.9 mmol/l; aldosterone+G-36 EC50= 29.0 ± 2.1 mmol/l; n= 7; P< 0.001). Finally, we found that the sensitization of CTGF by aldosterone was mediated, at least in part, by the sodium/hydrogen exchanger (NHE). We conclude that aldosterone in the CNT lumen sensitizes CTGF via a nongenomic effect involving GPR30 receptors and NHE. Sensitized CTGF induced by aldosterone may contribute to renal damage by increasing Af-Art dilation and glomerular capillary pressure (glomerular barotrauma).

Nonadherence to inhaled corticosteroids (ICSs) for asthma maintenance therapy is common and is associated with poor asthma outcomes. Simplifying dosing regimens for some chronic disease conditions has resulted in better adherence; however, little is known regarding the effect of ICS dosing on adherence for the treatment of asthma.

Although depression has been linked with asthma, its relationship with asthma exacerbations, including emergency department (ED) visits and oral steroid (OS) use, has not been well documented. The aim is to investigate whether depression increases exacerbations among patients with asthma.

Parathyroid hormone (PTH) is positively coupled to the generation of cAMP via its actions on the PTH1R and PTH2R receptors. Renin secretion from juxtaglomerular (JG) cells is stimulated by elevated intracellular cAMP, and every stimulus that increases renin secretion is thought to do so via increasing cAMP. Thus we hypothesized that PTH increases renin release from primary cultures of mouse JG cells by elevating intracellular cAMP via the PTH1R receptor. We found PTH1R, but not PTH2R, mRNA expressed in JG cells. While PTH increased JG cell cAMP content from (log10means ± SE) 3.27 ± 0.06 to 3.92 ± 0.12 fmol/mg protein (P< 0.001), it did not affect renin release. The PTH1R-specific agonist, parathyroid hormone-related protein (PTHrP), also increased JG cell cAMP from 3.13 ± 0.09 to 3.93 ± 0.09 fmol/mg protein (P< 0.001), again without effect on renin release. PTH2R receptor agonists had no effect on cAMP or renin release. PTHrP increased cAMP in the presence of both low and high extracellular calcium from 3.31 ± 0.17 to 3.83 ± 0.20 fmol/mg protein (P< 0.01) and from 3.29 ± 0.18 to 3.63 ± 0.22 fmol/mg protein (P< 0.05), respectively, with no effect on renin release. PTHrP increased JG cell cAMP in the presence of adenylyl cyclase-V inhibition from 2.85 ± 0.17 to 3.44 ± 0.14 fmol/mg protein (P< 0.001) without affecting renin release. As a positive control, forskolin increased JG cell cAMP from 3.39 ± 0.13 to 4.48 ± 0.07 fmol/mg protein (P< 0.01) and renin release from 2.96 ± 0.10 to 3.29 ± 0.08 ng ANG I·mg prot−1·h−1(P< 0.01). Thus PTH increases JG cell cAMP via non-calcium-sensitive adenylate cyclases without affecting renin release. These data suggest compartmentalization of cAMP signaling in JG cells.

Increasing Na delivery to the connecting tubule (CNT) causes afferent arteriole (Af-Art) dilation, a process we call CNT glomerular feedback (CTGF). Angiotensin II (ANG II) in the CNT lumen enhances CTGF via PKC. We hypothesized that luminal ANG II stimulates CTGF via activation of protein kinase C (PKC), NADPH oxidase 2 (NOX2), and enhanced production of superoxide (O2−). Rabbit Af-Arts and adherent CNTs were microdissected and microperfused in vitro. Dilation of the Af-Art was induced by increasing luminal CNT NaCl from 0 to 5, 10, 30, 45, and 80 mM, and the concentration of NaCl that elicited a half-maximal response (EC50) was calculated. Compared with vehicle, adding ANG II (10−9M) to the CNT lumen reduced EC50from 37 ± 3 to 14 ± 1 mM (P< 0.001), indicating ANG II potentiates CTGF. In the presence of ANG II, the O2−scavenger tempol (10−4M) increased EC50from 20 ± 4 to 41 ± 3 mM (P< 0.01), the NOX inhibitor apocynin (10−5M) increased EC50from 17 ± 2 to 39 ± 4 mM (P< 0.01), and the specific NOX2 inhibitor gp91ds-tat (10−5M) increased EC50from 19 ± 2 to 34 ± 2 mM (P< 0.01). However, tempol, apocynin, and gp91ds-tat had no effect on CTGF in the absence of ANG II. Compared with vehicle, the PKC activator PMA (2 × 10−7M) decreased EC50from 35 ± 2 to 14 ± 1 (P< 0.001). In the presence of PMA, tempol increased EC50from 14 ± 2 to 35 ± 2 mM (P< 0.01). We conclude the PKC/NOX2/O2−pathway mediates the enhancement of CTGF by luminal ANG II but it does not participate in CTGF in the absence of ANG II.

-Blockers (BB) are a mainstay of heart failure (HF) treatment, yet there are inconclusive data regarding their efficacy in African American individuals.

Pregnancy alters the function of many body systems, including the immune system. However, little is known regarding the effect of pregnancy on maternal IgE levels or atopy.

Previous studies suggest that small antigen doses given frequently are more likely to induce IgE production than are large antigen doses given infrequently.

US national guidelines recommend assessing short-acting ß-agonist (SABA) medication use as a marker of asthma severity and control. However, the relationship between recent SABA use and asthma exacerbations is not currently known.

Innate immune system stimuli, such as endotoxin, seem to affect allergy risk. Previously, we described gene-environment interactions between the endotoxin receptor polymorphism C-260T of the CD14gene and endotoxin exposure on total serum IgE level; however, the mechanism of this interaction is not known.

Regular use of inhaled corticosteroids (ICSs) can improve asthma symptoms and prevent exacerbations. However, overall adherence is poor among patients with asthma.

Family history is an important risk factor for atopic disease. However, most studies assess only limited information on family history. Because atopic disease can exhibit transient or persistent patterns, it may be useful to assess information on patterns of disease within families. This approach has been applied in other diseases, such as cancer, to discriminate between predominately inherited versus environmentally caused (sporadic) cases.

Indoor dust mite and cat allergens have been related to the risk of atopic conditions. If allergen levels are influenced by modifiable residential characteristics, potential interventions to prevent disease could be deployed.

Several studies have suggested that exposure to house-dust mite (HDM) allergen in infancy increases the risk of developing asthma.

The accurate diagnosis of hypersensitivity to natural rubber latex is the initial step in the effective management of individuals with latex allergy and in ensuring the quality of epidemiologic studies. The diagnostic algorithm used in the evaluation of an individual with suspected latex allergy begins with a comprehensive clinical history during which risk factors (atopy, food allergies, hand dermatitis) and temporal relationships between symptoms and natural rubber product exposure are identified. If type IV hypersensitivity is suspected because of the delayed nature (hours to days) and confinement of symptoms to the skin-latex product contact areas, patch testing can be conducted to confirm the presence of activated T cells with specificity for rubber chemicals. If type I hypersensitivity is suspected because of ocular, upper and lower airway, and/or systemic symptoms that have rapid onset (minutes) after a definable latex exposure, a confirmatory skin or blood test for IgE antibody may be conducted to verify a state of sensitization within the individual. The definitive diagnosis would then be made only after consideration of the individual's clinical history and confirmatory in vivo and/or in vitro laboratory test results. If discordance remains between highly convincing latex-associated symptoms as identified in the history and repetitively negative confirmatory IgE antibody test results, then one of several types of in vivo provocation tests may be performed for adjudication. This overview examines the current state of the art in both in vivo and in vitro diagnostic methods for latex-specific IgE antibody detection in skin and blood. The performance, advantages, and limitations of each diagnostic method are compared. (J Allergy Clin Immunol 2002;110:S47-56.)

Graphical representation of statistical results is often used to assist readers in the interpretation of the findings. This is especially true for survival analysis where there is an interest in explaining the patterns of survival over time for specific covariates. For fixed categorical covariates, such as a group membership indicator, Kaplan‐Meier estimates (1958) can be used to display the curves. For time‐dependent covariates this method may not be adequate. Simon and Makuch (1984) proposed a technique that evaluates the covariate status of the individuals remaining at risk at each event time. The method takes into account the change in an individual's covariate status over time. The survival computations are the same as the Kaplan‐Meier method, in that the conditional survival estimates are the function of the ratio of the number of events to the number at risk at each event time. The difference between the two methods is that the individuals at risk within each level defined by the covariate is not fixed at time 0 in the Simon and Makuch method as it is with the Kaplan‐Meier method. Examples of how the two methods can differ for time dependent covariates in Cox proportional hazards regression analysis are presented. Copyright © 2002 Whurr Publishers Ltd.

Racial disparities in asthma prevalence are not fully explained. Previous studies have reported an association between low birth weight (LBW) and asthma. African-Americans are at a heightened risk for both conditions.

AbstractOccupational exposure to specific metals (manganese, copper, lead, iron, mercury, zinc, aluminum and others) appears to be a risk factor for Parkinson’s disease (PD) in some, but not all, case-control studies. These epidemiological studies are reviewed. Several methodological issues that may account for the lack of unanimity of findings are discussed, and suggestions for improved case-control methodology are offered. The study of the neurological disease outcome of workers who have had long-term, well-defined occupational exposure to one or more metals is also urged, with collaborative work including industrial hygienists, occupational toxicologists, neurologists, epidemiologists and biostatisticians. Such efforts, employing state-of-the-art case and control ascertainment and enrollment from suitable population bases, neurological diagnostic rigor and exposure assessment, will help to further define the potentially important roles played by metals in PD and other neurodegenerative disorders.

To determine whether an inverse dose-response relationship exists between cigarette smoking and PD among ever-smokers and ex-smokers.

AbstractParkinson’s disease (PD) is likely a result of both inherited and exogenous factors. In a study of 144 PD cases and 464 controls, we used PD family history as a surrogate for inherited PD susceptibility. Cases were more likely to report a first- or second-degree relative with PD: 16.0 vs. 4.3%; odds ratio (OR) = 4.2; 95% confidence interval (CI) = 2.3–7.6. A PD family history was a greater risk factor for PD in subjects under age 70 (OR = 8.8; 95% CI = 3.4–22.8) compared with those over 70 (OR = 2.8; 95% CI = 1.3–6.1) and in men (OR = 8.1; 95% CI = 3.4–19.2) compared with women (OR = 2.6; 95% CI = 1.1–6.0). We also tested whether a PD family history modified the effects of other PD risk factors. In subjects with a PD family history, occupational exposure to copper, lead or iron increased the risk for PD (OR = 3.0; 95% CI = 0.7–13.3), but this was not the case for those without a family history (OR = 1.1; 95% CI = 0.7–1.6). Ever smoking cigarettes was inversely associated with PD in those without a PD family history (OR = 0.6; 95% CI = 0.4–0.9), but was positively associated with PD in those with a PD family history (OR = 1.7; 95% CI = 0.5–5.9). In summary, our results suggest that a PD family history, and perhaps, therefore, an inherited susceptibility, confers a greater risk for PD in men and individuals under 70 years of age and may modify the effects of environmental risk factors for PD.