Effect of water calcium, copper, and silver on branchial Na+ permeability in a characid and cichlid fish.

We tested the hypothesis that water Ca2+ is involved in control of branchial Na+ permeability in low pH tolerant convict cichlids and black neon tetras. We measured Na+ efflux in water with different Ca2+ concentrations during exposure to low pH, silver, and copper, at levels which are known to stimulate Na+ efflux. For convict cichlids at pH 7.5 exposure to 0 µmol L-1 Ca2+caused Na+ efflux to rise 2.5 times above controls at 100 µmol L-1 Ca2+. However, raising [Ca2+] to 500 µmol L-1 had no effect. Upon exposure to pH 3.5 (control [Ca2+]) Na+ efflux rose almost 5× and increasing the [Ca2+] 5-fold did not reduce the magnitude of stimulation. Exposure to 1 µmol L-1 silver and 25 µmol L-1 copper stimulated Na+ efflux 7×, and 2×, respectively. Raising [Ca2+] concentration during metal exposure halved the stimulation of Na+ efflux caused by silver, and eliminated the stimulation elicited by copper. For black neon tetras raising or lowering water [Ca2+] had no effect on Na+ efflux at pH 7.5. Exposure to pH 3.5 caused Na+ efflux to rise 2.5× but changing [Ca2+] had no effect. Exposure to 1 µmol L-1 silver, or 25 µmol L-1 copper caused Na+ efflux of tetras to rise 4-fold and 3-fold, respectively. Raising [Ca2+] during silver exposure reduced the stimulation of Na+ efflux by about 50%, but during copper exposure increased [Ca2+] had no effect on stimulation of Na+ efflux. These results suggest water Ca2+ plays a role in control of branchial Na+ permeability in cichlids, but perhaps not tetras. In addition, the silver and copper concentrations required to inhibit Na+ uptake and stimulate Na+ efflux were higher than the concentrations used on non-characids and non-cichlids, which indicates that our fish are much more tolerant of these metals.

Characterization of genes expressed in mesophyll protoplasts of Nicotiana sylvestris before the re-initiation of the DNA replicational activity.

To decipher the early events preceding the re-entry of somatic cells into the cell cycle, we constructed a cDNA library from 6-h-old protoplasts of Nicotiana sylvestris. We characterized three mRNAs, via their cDNAs, that accumulate at very high levels 6 h after the beginning of the culture. Two of them could be identified by comparison of the deduced amino acid sequence to databanks. 6P10 is a novel type I trypsin inhibitor, which has the peculiarity of being devoid of the pro-sequence peptide described to be essential for transport to the vacuole. 6P73 is a novel, moderately anionic peroxidase. 6P50 belongs to a gene family not yet identified. These genes are highly expressed in protoplasts at the beginning of the culture and moderately in roots, but are neither expressed in response to chemical treatment, heat shock, pathogen attacks nor during tumor induction. These findings suggest that the activation of these genes corresponds not only to a specific adaptation of protoplasts to the new environment but also, since their level of expression decreases at the onset of division, to a sequence of events connected with the establishment of the new program of gene expression of the dividing cell.

Structure and promoter activity of a stress and developmentally regulated polyubiquitin-encoding gene of Nicotiana tabacum.

A polyubiquitin-encoding gene was identified from a Nicotiana tabacum genomic library using a specific probe spanning the 3' untranslated region of the corresponding cDNA. The gene, Ubi.U4, is expressed in various amounts in the whole plant, except in just-fully-expanded leaves. Genomic blots indicate that it originates from N. tomentosiformis. Sequence analyses reveal that the gene consists of four ubiquitin monomers extended by a fifth truncated subunit. It is disrupted by a single 457-bp intron in close proximity to the start codon of translation. Primer extension experiments localized the transcription start point (tsp). Transient gene expression in N. tabacum protoplasts indicates that the deletion of the intron has no significant influence on gene expression. Mutagenesis on putative cis-regulatory elements indicates at least three important motifs in the proximal promoter: an 'ACGT' core element, an A + T-rich sequence and a less clearly defined cis-element located between bp -162 and -113.

Phantom bite syndrome.

Despite repeated treatment failures, some individuals seek bite correction from a succession of dentists. Their pathological narcissism focuses on their bite, in a manner reminiscent of phantom limb phenomena. The dentist's diagnosis and treatment are manipulated until the patient claims them a failure and consults another dentist. The author suggests that this behavior represents a defense against paranoia and severe personality disorders.

Depression, anhedonia and anxiety in temporomandibular joint and other facial pain syndromes.

Depression, anhedonia, state anxiety (A-state), trait anxiety (A-trait), and self-reported pain estimate were measured in almost 500 facial pain patients. These patients were divided into 3 diagnostic categories: myofacial pain dysfunction syndrome (MPD) [18], arthritis of the temporomandibular joints (TMJ arthritis), and trigeminal neuralgia. Three control groups were measured for comparison. They consisted of an normal, or non-patient group, a group of arthritis patients, and a group of movement disorder patients attending a neurology clinic. Among the facial pain patients and the normal controls few differences were found with regard to anhedonia and depression, The arthritis and neurology patients produced significantly higher depression and anhedonia scores than did several of the facial pain groups. Pain estimate ranged from 0 for control, to a mean of 67.6 +/- 31.3 for the trigeminal neuralgia patients with the MPD (means = 56.2 +/- 32.5) and the TMJ arthritis patients (means = 46.7 +/- 30.8) somewhat lower. Clinical variables such as duration of pain, help seeking behavior and total number of symptoms were correlated with depression but not with anhedonia scores, It is hypothesized that anhedonia is a measure separate from depression and may be more closely linked to suffering behavior that to pain behavior. Psychological variables did not discriminate among facial pain patients and in particular did not distinguish between so-called functional and organic illness.

Why is depression comorbid with chronic myofascial face pain? A family study test of alternative hypotheses.

A number of explanations have been proposed to account for findings that rates of depression are elevated in persons with chronic, non-malignant pain disorders (CNPDs); for example, that CNPDs are variants of depression (e.g. 'masked depression'), that the stress of living with CNPDs contribute to the onset of depression ('diathesis-stress'), or that the correlation of CNPDs and depression is a methodological artifact of studying treatment-seeking samples. These alternative hypotheses are tested for one specific CNPD, chronic myofascial face pain, using a family study methodology. The procedure was to conduct direct psychiatric interviews with 106 patients with a history of carefully diagnosed myofascial face pain, 118 acquaintance controls without personal histories of myofascial face pain, and a random sample of adult first degree relatives of these case and control probands. The probands were further subdivided into four roughly equal samples consisting of cases with and without personal histories of major depressive disorder (MDD), and controls with and without personal histories of MDD. Dates of initial onsets of myofascial face pain and MDD in patient probands were obtained from interviews and records. The main results were that, compared to control probands without personal histories of MDD, MDD and depressive spectrum disorders (DSD) were elevated in the first degree relatives of control probands with personal histories of early onset MDD, but not in the first degree relatives of myofascial face pain probands with or without personal histories of early or late onset MDD. This outcome is consistent with the hypothesis that living with chronic myofascial face pain contributes to elevated rates of depression. It is inconsistent with the alternative hypotheses that this CNPD is a variant of depression or that the elevated MDD rates are simply an artifact of selection into treatment. The implications of these results and additional results consistent with them are discussed.

Myofascial TMD does not run in families.

This study tests whether facial pain or associated symptoms and disorders aggregates in first degree relatives of those with myofascial temporomandibular disorders (M/TMD). We randomly selected one first degree relative of 106 probands with a lifetime history of M/TMD and one first degree relative of 118 acquaintance control probands with no history of M/TMD. Relatives were directly interviewed about the lifetime occurrence of a broad range of painful and non-painful health conditions and symptoms. Analyses revealed that rates of facial pain, symptoms of TMDs, and a range of other musculoskeletal conditions were not significantly different in first degree relatives of M/TMD probands and first degree relatives of controls. In addition, proband descriptors of facial pain severity or disability did not significantly predict the likelihood of having a first degree relative with one or more TMD-related symptoms. These results indicate that M/TMD is not a familial disorder.

Why are quiescent mesophyll protoplasts from Nicotiana sylvestris able to re-enter into the cell cycle and re-initiate a mitotic activity?

Mesophyll protoplasts of Nicotiana sylvestris incubated in an adequate culture medium re-enter very rapidly into the cell cycle and divide. The transition G0/G1 is accompanied by a complete reversion of the program of gene expression. The program of the photosynthetic differentiated mesophyll cell is abolished whereas a new multipartite program of a highly stressed but ready-to-divide cell is established. Some genes encode proteins which structure suggests they may play key roles in these events. Most of the induced genes are under multiple controls: stress and/or development. Stress response and cellular re-organization might thus be closely related events that cannot be dissociated. It is probable that the re-entry of a protoplast into the cell cycle, ie the initial step of totipotency, closely depends on the coordinated activation of a set of genes that share common regulatory mechanisms.

Temporomandibular pain and dysfunction syndrome. History, physical examination, and treatment.

A stepwise method for treating TMPDS is presented. Step 1-start patient on a regimen of chloroethane or chlorofluorocarbon spray and exercise. Step 1A--if a clicking joint is the chief complaint, start with click exercise. Step 1B--if restricted mouth opening is the chief complaint, start with range of motion exercise; employ exercises sequentially, not simultaneously. Step 2--if pain is moderate to severe, start with amitriptyline 10 mg at bedtime, increasing the dose in 10-mg increments to 40 mg. Step 3--for nonresponders, add injections of tender points with lidocaine and consider a trial of a different tricyclic. Step 4--for nonresponders, consider a trial of tender point injections combining dexamethasone with local anesthetic. Start by injecting the three most painful tender points with 0.5 mL of a solution of 1 mg of dexamethasone combined with two thirds bupivacaine and one third lidocaine to reach the desired volume. Repeat injections, varying the sites as required. Do this once weekly for 4 to 6 weeks for an adequate trial. This regimen can be continued for an extended period of time with appropriate precautions in place. The value of judgment-free psychosocial support cannot be overemphasized. Patients with TMPDS are faced with long-term problems of pain management. An understanding clinician can provide the sustained support required to prevent the cycle of ever more invasive treatments with their potential for harm.

Heat stress does not modify lactate exchange and removal abilities during recovery from short exercise.

Arterial and femoral venous lactate concentrations were measured before, during, and after short intermittent exercise (55-118% of maximal O2 consumption) in thermoneutral (N, 25 degrees C, 10.5 Torr) and hot (H, 45 degrees C, 17.5 Torr) conditions. The thermal load induced significantly higher heart rate and rectal temperature in H relative to N. All the arterial lactate (La) recovery curves were fitted to an equation containing two exponential time functions of the form La(t) = La(0) + A1a(1 - e-gamma 1at) + A2a(1 - e-gamma 2at) where the velocity constants gamma 1a and gamma 2a are the body's overall ability to exchange and remove lactate after exercise, respectively, and t is time. There was no significant difference in these constants, regardless of thermal conditions. The arterial lactate concentration at the end of exercise, the peak lactate concentration during recovery, the amplitudes A1a and A2a of the biexponential function, and the arteriofemoral venous lactate concentration difference during recovery were not significantly different in H relative to N. However, measured and computed arterial lactate concentrations during recovery, especially at the end of the tests, were higher in H (P < 0.04). The more elevated lactate concentrations in H at rest at the end of recovery denote a higher basal lactate production, and they were not due to muscle hypoxia.

Work rate-dependent lactate kinetics after exercise in humans.

Arterial blood lactate concentrations were measured on 19 subjects before, during, and after a 3-min bicycle exercise at several work rates, and the concentrations during the recovery phases were fitted to a biexponential time function consisting of a rapidly increasing and a slowly decreasing component. Highly significant correlations with the work rate of the exercise preceding the recovery were found for all the parameters of the fitted equation. The two velocity constants show inverse linear relationships, whereas the other parameters vary according to a definite power function. A functional meaning has been given to the two velocity constants, namely the ability of the tissues to exchange and to remove lactate. For the group of subjects studied, after exercises at work rates below about 3.5 W/kg, the tissue's ability to utilize, and possibly to exchange lactate, increases over values generally reported for resting conditions, whereas after exercises at higher work rates the inverse occurs. Lactate kinetics during recovery appear to be the result of two underlying processes, one enhancing the ability of the tissues to exchange and remove lactate and the other restraining it.

Lactate removal ability and graded exercise in humans.

Venous lactate concentrations of nine athletes were recorded every 5 s before, during, and after graded exercise beginning at a work rate of 0 W with an increase of 50 W every 4th min. The continuous model proposed by Hughson et al. (J. Appl. Physiol. 62: 1975-1981, 1987) was well fitted with the individual blood lactate concentration vs. work rate curves obtained during exercise. Time courses of lactate concentrations during recovery were accurately described by a sum of two exponential functions. Significant direct linear relationships were found between the velocity constant (gamma 2 nu) of the slowly decreasing exponential term of the recovery curves and the times into the exercise when a lactate concentration of 2.5 mmol/l was reached. There was a significant inverse correlation between gamma 2 nu and the rate of lactate increase during the last step of the exercise. In terms of the functional meaning given to gamma 2 nu, these relationships indicate that the shift to higher work rates of the increase of the blood lactate concentration during graded exercise in fit or trained athletes, when compared with less fit or untrained ones, is associated with a higher ability to remove lactate during the recovery. The results suggest that the lactate removal ability plays an important role in the evolution pattern of blood lactate concentrations during graded exercise.

The examination of myofascial face pain and its relationship to psychological distress among women.

In this study, 110 female myofascial face pain patients were assessed monthly for 10 months on measures of pain, distress, and stressful life events. D. A. Kenny and A. J. Zautra's (1995) structural equation model for examining the separate trait, state, and error components of the variables was used to analyze the data. Both pain and distress had sizable trait variance, and the trait components were correlated. The 2 variables also showed sizable state variance, and the states of pain covaried with states of distress. A significant time-lagged relationship between the 2 variables was found: Increases in distress led to elevations in pain 1 month later. Stressful life events arising from major social roles were also associated with greater distress, but not pain. Illness events unrelated to the pain syndrome were associated with both pain and distress.

Medically unexplained chronic orofacial pain. Temporomandibular pain and dysfunction syndrome, orofacial phantom pain, burning mouth syndrome, and trigeminal neuralgia.

Orofacial pain syndromes pose a dilemma for physicians. Even when the patient is referred, quality medical care requires that the physician be acquainted with current evidence-based practice. Such practice may be radically different from the traditional view. This article reviews the differential diagnosis and treatment of the most common medically unexplained orofacial syndromes.

Scattered photons as the cause for the observed dmax shift with field size in high-energy photon beams.

Measurements on the Sagittaire linear accelerator and Allis-Chalmers betatron at M. D. Anderson Hospital indicate that the observed dmax shift with field size is due to the presence of Compton-scattered photons in the therapy beam, and not electrons as proposed by others. Separating the primary from other radiation components indicates that the secondary fraction represents a percentage contribution to the overall beam that increases as the collimators are opened. This is consistent with what would be expected from Compton scattering and explains the effective softening of the beam as field size increases.

Management of radiation oncology patients with implanted cardiac pacemakers: report of AAPM Task Group No. 34. American Association of Physicists in Medicine.

Contemporary cardiac pacemakers can fail from radiation damage at doses as low as 10 gray and can exhibit functional changes at doses as low as 2 gray. A review and discussion of this potential problem is presented and a protocol is offered that suggests that radiation therapy patients with implanted pacemakers be planned so as to limit accumulated dose to the pacemaker to 2 gray. Although certain levels and types of electromagnetic interference can cause pacemaker malfunction, there is evidence that this is not a serious problem around most contemporary radiation therapy equipment.

Comorbid fibromyalgia accounts for reduced fecundity in women with myofascial face pain.

OBJECTIVE: This study examined factors related to reduced fecundity among women with myofascial face pain (MFP) arising from hypotheses concerning the role of neurohormonal factors in MFP and associated conditions. DESIGN: Fecundity rates among 162 MFP cases and 173 demographically equivalent acquaintance female controls were compared. OUTCOME MEASURES: Fecundity indicators and factors underlying differential fecundity rates were investigated. RESULTS: It was determined that female cases with MFP had significantly fewer children and were more likely to have never been pregnant. Although women with MFP were more likely than controls to indicate that volitional factors related to their health discouraged them from any or additional pregnancies, these factors did not account for lower rates of fecundity. MFP cases also did not differ from controls on self-reported indicators of infertility. Moreover, we show that reduced fecundity was restricted to the subgroup of MFP cases who reported a history of fibromyalgia. CONCLUSIONS: Reduced fecundity in women with MFP is restricted to those who self-report a history of fibromyalgia. Possible mechanisms for reduced fecundity in fibromyalgia are discussed. These findings highlight the need to screen for widespread pain among women with regional myofascial pain syndromes.

When did your pain start?: reliability of self-reported age of onset of facial pain.

OBJECTIVE: This study was designed to examine the reliability of self-reported onset of facial pain over a relatively long period, as well as factors that may influence the ability of patients to provide consistent pain onset dates. The implications of dating unreliability on assessing the temporal order of two potentially related disorders is also considered. DESIGN: A total of 125 women with a lifetime history of temporomandibular pain and dysfunction syndrome (TMPDS) were asked to report their pain onset date in the context of a structural health interview. Dates were compared with onset dates recorded an average of 7 years earlier in their clinical chart. Factors potentially affecting reliability of recall were also assessed. RESULTS: The absolute value of the discrepancy between the two reports was nearly 4 years. Only 26% reported onset dates within the same year. Forward-telescoping, in which events are recalled as occurring more recently than they actually occurred, was more common than backward-telescoping of onset dates. Intraclass correlations were good to excellent (ICC = .80 for full sample). Elapsed time between reports was the largest predictor of reporting discrepancy. CONCLUSIONS: These findings indicate that a single patient's report of pain onset, especially when he or she is asked to recall the onset of a long-standing pain problem, will most often lead to an underestimate of chronicity. However, high intraclass correlations indicate that patients' dating of pain onset may have satisfactory reliability for research purposes, when comparing a group of patients to one another to assess relative chronicity of pain.

The control group conundrum in chronic pain case/control studies.

The choice of an appropriate control group has been recognized as one of the most difficult problems in the methodology of case/control studies, both in theory and in practice. In the study of chronic pain, a "well control group" has frequently been employed. Although this design has intuitive appeal, it contains the potential for bias and error. In order to obtain the proper control group, the same exclusion criteria should be applied to cases and controls. Second, controls should be selected independently of exposure to the putative risk factors under investigation. To illustrate the nature of this problem we present two numerical examples, using a chronic pain disorder.

Is major depression comorbid with temporomandibular pain and dysfunction syndrome? A pilot study.

There is a lack of information about the precise strength of the relationship between chronic pain and depression. In a prior study, women with temporomandibular pain and dysfunction syndrome (TMPDS) had much higher scores than did controls on a measure of nonspecific psychological distress. The question arose as to whether rates of clinical depression are also unusually high in TMPDS patients. Their former treating clinician rates cases for likely lifetime presence or absence of depression. A subset of those rated as likely depressed then had their diagnoses verified independently through a structured clinical interview by a psychiatrist and clinical psychologist. Results revealed a minimum lifetime prevalence rate for major depression of 41%. A rate of this magnitude in TMPDS cases is clearly much higher than would be found for women of similar background in the general population.