Comparative evaluation of therapeutic efficacy and safety of black peel versus 25% trichloroacetic acid peel in mild to moderate acne vulgaris: a split face study.

Introduction: Peeling has withstood the test of time as a simple, minimally invasive method to renew the skin, despite the introduction of more advanced procedures like lasers. Materials and Methods: Thirty patients (or 60 sites) with age ranging from 15 to 45 years with mild-to-moderate acne vulgaris were included in the study. Assessment at baseline was done by the global acne grading system score for including mild and moderate acne patients. Results: On grading the improvement according to the 5-point Global Assessment Scale (GAS), it was found that in area A (black peel), 6.7% of patients showed excellent improvement, 86.7% of patients showed good improvement, and 6.7% of patients showed fair improvement. In area B (25%TCA peel), 6.7% of patients showed excellent improvement, 80% of patients showed good improvement, and 13.3% of patients showed fair improvement. Discussion: None of the patients showed poor or worse outcomes in any of the areas. The difference between the groups was not significant (P = 0.688). Conclusion: There is a paucity of data in the literature regarding the comparison of black peel with other conventional peels in the treatment of acne vulgaris. To the best of our knowledge, this is the first study comparing black peel with TCA peel in the treatment of acne vulgaris.

Comparative Evaluation of Efficacy and Safety of Tacrolimus and Dinoprostone Following Dermabrasion in Stable Vitiligo.

BACKGROUND: Dinoprostone (DNP), a prostaglandin E2 (PGE2) analogue, has been found to cause repigmenation in vitiliginous lesions. Combined medical and surgical therapy might be more useful for successful treatment of vitiligo. OBJECTIVES: In this study, we aimed to evaluate the efficacy and safety of dermabrasion followed by dinoprostone gel and to compare it with tacrolimus ointment following the same procedure in the treatment of localized stable vitiligo. METHODS: 40 patients of stable vitiligo were enrolled which were divided in two groups of 20 patients each. In group 1, dermabrasion followed by tacrolimus 0.1% ointment was done and in group 2, dermabrasion followed by dinoprostone gel was done. RESULTS: Group 1 patients showed slightly better response (P=0.039), whereas the side effect profile was better for group 2. CONCLUSION: DNP and tacrolimus have immunomodulatory and melanocyte stimulating effect and are well tolerated when combined with dermabrasion. Their effect on skin pigmentation could be enhanced by dermabrasion. J Drugs Dermatol. 2021;20(5):519-522. doi:10.36849/JDD.5751.

Comparative Evaluation of the Therapeutic Efficacy and Safety of Injected Histaglobulin versus Autologous Serum Therapy in Chronic Urticaria.

BACKGROUND: Urticaria affects 0.5 to 1 percent of the population at any given time. Treatments include nonsedative antihistamines, autologous serum therapy, and injected histaglobulin. OBJECTIVE: This study sought to compare the therapeutic efficacy and safety of injected histaglobulin with autologous serum therapy in chronic urticaria. METHODS: This was a hospital-based prospective study performed in the Department of Dermatology, Venereology, and Leprology at Guru Gobind Singh Medical College and Hospital in Faridkot, India. A total of 96 patients with chronic idiopathic urticaria were enrolled after applying inclusion and exclusion criteria and were divided into two groups of 48 patients each using an envelope method. Autologous serum skin tests were performed in each patient irrespective of their group assignment. Group A then received injected histaglobulin and Group B received autologous serum therapy (AST). Patient were evaluated using the Urticaria Activity Score (UAS) every week for six weeks, with follow-up conducted at three and six weeks after the completion of treatment. The Chronic Urticaria Quality of Life questionnaire was used to assess the quality of life of the study participants. RESULTS: Out of the 96 initially enrolled patients, 62 completed the six weeks of treatment and two follow-up visits. Twenty patients dropped out due to remission and 14 patients left the study for other reasons. Reductions in UAS values occurred in both the groups by the end of follow-up but were more significant in Group A. Improvement in quality of life scores was also greater in Group A. Recurrence occurred in both groups after treatment cessation but was less common in Group A. CONCLUSION: Both treatments were validated for treating chronic urticaria; however, injected histaglobulin showed statistically more consequential results than AST.

The Histopathology of Oral Cancer Pain in a Mouse Model and a Human Cohort.

Oral cancer patients often have severe, chronic, and mechanically induced pain at the site of the primary cancer. Oral cancer pain is initiated and maintained in the cancer microenvironment and attributed to release of mediators that sensitize primary sensory nerves. This study was designed to investigate the histopathology associated with painful oral cancers in a preclinical model. The relationship of pain scores with pathologic variables was also investigated in a cohort of 72 oral cancer patients. Wild-type mice were exposed to the carcinogen, 4-nitroquinoline 1-oxide (4NQO). Nociceptive (pain) behavior was measured with the dolognawmeter, an operant device and assay for measuring functional and mechanical allodynia. Lesions developed on the tongues and esophagi of the 4NQO-treated animals and included hyperkeratoses, papillomas, dysplasias, and cancers. Papillomas included lesions with benign and dysplastic pathological features. Two histologic subtypes of squamous cell carcinomas (SCCs) were identified-SCCs with exophytic and invasive components associated with papillary lesions (pSCCs) and invasive SCCs without exophytic histology (iSCCs). Only the pSCC subtype of tongue cancer was associated with nociceptive behavior. Increased tumor size was associated with greater nociceptive behavior in the mouse model and more pain experienced by oral cancer patients. In addition, depth of invasion was associated with patient-reported pain. The pSCC histology identifies 4NQO-induced tongue cancers that are expected to be enriched for expression and release of nociceptive mediators.

Bluetongue virus vaccine: conventional to modern approach.

Bluetongue (BT) is an economically important, infectious and non-contagious disease of ruminant animals. BT disease is caused by bluetongue virus (BTV) of the genus Orbivirus (the family Reoviridae). BTV is transmitted by certain species of biting midges of the genus Culicoides. Although originally BT was restricted to African continent, now it is present in all the continents except Antarctica. Conventional BT vaccines such as live attenuated and inactivated vaccines showed different degree of success in BT control. However, conventional vaccines have certain disadvantages of reversion to virulent strain and frequent booster dose requirement. Several BT outbreaks in India and the rest of the world open a new insight for development of better vaccines. The development in molecular biology techniques allowed the development and validation of several modern vaccines such as subunit vaccine, recombinant vector vaccine, disabled infections single cycle (DISC) vaccine, differentiating infected from vaccinated animals (DIVA) approach etc. Most of these vaccines are considered as safer, having better protective immune response and provided cross-protective immunization against more than one serotype. Keywords: bluetongue virus; live vaccine; inactivated vaccine; DISC; recombinant vaccine.

Are procedures performed by dental auxiliaries safe and of comparable quality? A systematic review.

The objective of the current study was to systematically evaluate the existing evidence in relation to the safety, quality, productivity or cost-benefit, and patient satisfaction of the procedures performed by the different groups of dental providers. Due to the diversity of the procedures performed and the outcomes measured, it was not possible to create pooled estimates in a meaningful manner. Therefore, summary results of individual studies are presented and critically evaluated.

Blepharochalasis--a rare entity.

We report a case of a 9-year-old boy with blepharochalasis, who had recurrent angioedema along with wrinkling of the skin of the upper eyelids since age 5 years. The systemic examination of the patient was normal. The patient was diagnosed as a typical case of blepharochalasis. Although the normal age to develop blepharochalasis is at puberty, our patient developed it, which is rare.

Pityriasis rosea unilateralis.

The classical pityriasis rosea presents with erythematous papulosquamous lesions. It has got many clinical and morphological variants. Pityriasis rosea unilateralis is very rare variant of pityriasis rosea. We are reporting two cases of unilateral pityriasis rosea.

Urocortin increases the expression of heat shock protein 90 in rat cardiac myocytes in a MEK1/2-dependent manner.

We have previously demonstrated that urocortin protects cultured cardiac myocytes from ischaemic and reoxygenation injury and decreases the infarct size in the rat heart exposed to regional ischaemia and reperfusion. Urocortin-mediated cardioprotection is via activation of the mitogen-activated protein kinase (MAP kinase, MEK1/2) pathway. In addition, it is well documented that heat shock protein (hsp) 70 and hsp90 are cardioprotective against lethal stress. In this study we show, for the first time, that urocortin induces the expression of hsp90 but not hsp70 in primary cultures of rat neonatal cardiac myocytes. Levels of hsp90 protein increase by 1.5-fold over untreated cells within 10 min of urocortin treatment and are sustained for 24 h with a maximal increase of 2.5-fold at 60 min (P<0.05 at all time points). The increase in hsp90 expression by urocortin was not inhibited by actinomycin D, and urocortin failed to increase hsp90 promoter activity. Urocortin induction of hsp90 was inhibited by the MEK1/2 inhibitor PD98059 (P<0.001) and by cycloheximide, and both inhibitors abrogate urocortin-mediated cardioprotection (P<0.05 for cycloheximide, P<0.001 for PD98059). Hence, MEK1/2 and protein synthesis are involved in the cardioprotective effect of urocortin against hypoxic-mediated cell death, possibly due to an increase in expression of hsp90 protein. This is the first report of heat shock protein induction by urocortin or any other member of the corticotrophin-releasing hormone family.

Bilateral herpes--Zoster of widely separated dermatomes in a non-immunocompromised female.

Herpes zoster involving simultaneously left maxillary dermatome and right 2nd lumbar dermatome in a non-immunocopromised 24-year-old female is being reported due to its rarity.

CT-1 mediated cardioprotection against ischaemic re-oxygenation injury is mediated by PI3 kinase, Akt and MEK1/2 pathways.

Cardiotrophin-1 protects cardiac myocytes from ischaemic re-oxygenation (IR) injury. CT-1 activates MEK1/2,p42/44MAPK as well as the phosphatidylinositol (PI) 3-OH kinase (PI3) protein kinase B (PKB/Akt) pathway. In this study we investigate the signalling pathways that mediate the anti-apoptotic cell survival effect of CT-1 in IR. Dominant negative gene based inhibitors of MEK1/2, PI3-kinase and Akt inhibited CT-1 mediated cardioprotection in re-oxygenation as did chemical inhibitors of the PI3-kinase pathway. Hence the PI3-kinase/Akt pathway is required in addition to MEK1/2 to mediate CT-1 cardioprotection in IR.

Cardioprotective effects of transforming growth factor-beta1 during early reoxygenation or reperfusion are mediated by p42/p44 MAPK.

Apoptosis contributes to myocardial cell death during ischemia and reperfusion, especially during reperfusion. Growth factor "survival" signaling attenuates apoptosis. We therefore examined the effects of transforming growth factor-beta1 (TGF-beta1) on reperfusion injury and assessed the role of p42/p44 MAPK signaling in TGF-beta1-induced protection. Rat ventricular myocytes were subjected to hypoxia and reoxygenation. TGF-beta1 (0.2 ng/ml) was applied to cells during reoxygenation and the extent of apoptosis was determined by TUNEL and annexin V binding assays. Further studies were conducted in intact rat hearts subjected to regional ischemia and reperfusion. TGF-beta1 (0.2 ng/ml) was perfused during early reperfusion. In cells, incubation with TGF-beta1 (0.2 ng/ml) during reoxygenation attenuated the extent of cell membrane damage (trypan blue uptake) and also reduced the numbers of TUNEL-and annexin V-positive cells. Reduction of apoptosis was abrogated by PD98059 (5 microM), an inhibitor of p42/p44 MAPK activation. TGF-beta1 activated p42/p44 MAPK transiently in normoxic myocytes. When intact hearts received TGF-beta1 (0.2 ng/ml) during early reperfusion, infarct size was reduced from 39.4 +/- 3.1% to 17.3 +/- 3.1% (p < 0.01). This protective action of TGF-beta1 was abrogated by PD98059. These studies are the first to show that TGF-beta attenuates cardiac myocyte apoptosis during early reperfusion and limits infarct size through p42/p44 MAPK activation.

The pharmacology of bimatoprost (Lumigan).

Bimatoprost (Lumigan) is a pharmacologically unique and highly efficacious ocular hypotensive agent. It appears to mimic the activity of a newly discovered family of fatty acid amides, termed prostamides. One biosynthetic route to the prostamides involves anandamide as the precursor. Bimatoprost pharmacology has been extensively characterized by binding and functional studies at more than 100 drug targets, which comprise a diverse variety of receptors, ion channels, and transporters. Bimatoprost exhibited no meaningful activity at receptors known to include antiglaucoma drug targets as follows: adenosine (A(1-3)), adrenergic (alpha(1), alpha(2), beta(1), beta(2)), cannabinoid (CB(1), CB(2)), dopamine (D(1-5)), muscarinic (M(1-5)), prostanoid (DP, EP(1-4), FP, IP, TP), and serotonin (5HT(1-7)). Bimatoprost does, however, exhibit potent inherent pharmacological activity in the feline iris sphincter preparation, which is prostamide-sensitive. Bimatoprost also resembles the prostamides in that it is a potent and highly efficacious ocular hypotensive agent. A single dose of bimatoprost markedly reduces intraocular pressure in dogs and laser-induced ocular hypertensive monkeys. Decreases in intraocular pressure are well maintained for at least 24 hr post-dose. Human studies have demonstrated that systemic exposure to bimatoprost is low and that accumulation does not occur. The sclera is the preferred route of accession to the eye. The high scleral permeability coefficient Papp is a likely contributing factor to the rapid onset and long-acting ocular hypotensive profile of bimatoprost.

Cardiotrophin-1 can protect cardiac myocytes from injury when added both prior to simulated ischaemia and at reoxygenation.

OBJECTIVE: The cytokine cardiotrophin-1 (CT-1) has previously been shown to protect cultured cardiocytes from cell death induced by serum removal or hypoxia when administered prior to the damaging stimulus. We wished to test whether a similar protective effect could be observed if CT-1 was added after the ischaemic period and to investigate the signalling pathways involved in the protective effect when CT-1 is given prior to or after ischaemia. METHODS: We therefore examined the protective effect of CT-1 in cultured rat cardiocytes exposed to simulated ischaemia followed by reoxygenation when CT-1 was administered either prior to simulated ischaemia or at reoxygenation. RESULTS: We show that CT-1 can exert a protective effect against the damaging effects of simulated ischaemia/reoxygenation both when added after the simulated ischaemia at reoxygenation (P<0.05 in trypan blue, TUNEL and annexin V assays) or when added prior to the simulated ischaemia (P<0.05). In both cases, these protective effects are blocked by an inhibitor of the p42/p44 MAPK pathway (P<0.05 in all assays). CONCLUSION: CT-1 can protect cardiac cells when added either prior to simulated ischaemia or at the time of reoxygenation following simulated ischaemia and these effects are dependent upon its ability to activate the p42/p44 MAPK pathway. Hence CT-1 may have therapeutic potential when added at the time of reperfusion following ischaemic damage.

Induction of apoptosis and Fas receptor/Fas ligand expression by ischemia/reperfusion in cardiac myocytes requires serine 727 of the STAT-1 transcription factor but not tyrosine 701.

Previously we reported that ischemia results in apoptosis and is accompanied by phosphorylation on Tyr-701 and increased expression and transcriptional activity of the signal transducer and activator of transcription-1 (STAT-1). In the present study, we show that exposure of cardiomyocytes to ischemia induced the phosphorylation of STAT-1 at another site, Ser-727. Moreover, STAT-1 is critical for the induction of Fas receptor and Fas ligand expression by ischemia/reperfusion (I/R). Transcriptional activation of Fas and FasL was dependent on Ser-727 of STAT-1 but was independent of Tyr-701. Similarly, Ser-727 but not Tyr-701 was required for enhancement of cardiomyocyte cell death by STAT-1 during I/R. In addition, inhibition of the p38 pathway prevented the induction and transcriptional activation of Fas and FasL in cardiac cells exposed to I/R, whereas inhibition of p42/p44 MAPK had no effect. Finally, I/R also induced phosphorylation of STAT-1 on Ser-727 and expression of Fas/FasL in ventricular myocytes in the intact heart ex vivo. These results indicate that Fas/FasL genes and apoptosis are activated by STAT-1 in cardiac myocytes exposed to I/R and these effects are dependent on the Ser-727 but not the Tyr-701 phosphorylation sites of STAT-1.

Feasibility of continuous transthoracic cardiac imaging using a novel ultrasound transducer.

BACKGROUND: The feasibility of hands-free transthoracic continuous ultrasonic cardiac imaging has not been demonstrated previously. We developed a 2.5-MHZ spherical transducer mounted in an external housing to permit steering in 360 degrees (CONTISON). The external housing was attached to the chest wall using an adhesive patch. METHODS AND RESULTS: The transducer was placed in the third or fourth interspace at the left sternal border to permit imaging of the left ventricle (LV) in its short axis and attached to the chest wall. The transducer then was attached to an ultrasound machine. Ten normal subjects and 20 patients with previous myocardial infarction were studied. The following maneuvers were performed at the beginning of the study: (1) The patient was rotated from the supine position (0 degrees ) in 20 degrees increments to the left lateral decubitus position (90 degrees ). The echocardiogram was displayed continuously and was recorded on videotape (parasternal short-axis view) at 0 degrees, 20 degrees, 40 degrees, 60 degrees, 80 degrees, and 90 degrees. (2) The patient was returned to the supine position and an echocardiogram was obtained. The patient was then seated up 20 degrees, 40 degrees, 60 degrees, 80 degrees, and 90 degrees by using the controls on the bed. (3) The patient then was returned to the supine position and the echocardiogram was displayed continuously on the monitor. The echocardiogram was recorded every 15 minutes for a period of 4 hours. All segments of the LV were visualized in the supine position and during lateral rotation (0 degrees -90 degrees ). Thus, body position did not affect the image. All segments of the LV were visualized during sitting up (0 degrees -90 degrees ), and all segments were visualized during the 4 hours of imaging. The patients were able to move around without distortion of the image. CONCLUSION: The CONTISON transducer permitted continuous imaging of LV wall motion. Body position did not affect interpretation of wall motion. This device has potential applicability in monitoring LV function in the intensive care setting.

Cardiotrophin-1 reduces stress-induced heat shock protein production in cardiac myocytes.

Cardiotrophin-1 (CT-1) can induce expression of the protective heat shock proteins (hsps) in cardiac cells. We show here that, unlike the stress induced accumulation of hsps, the effect of CT-1 is not accompanied by increased hsp mRNA levels and is insensitive to the RNA synthesis inhibitor actinomycin D, suggesting that it occurs at the post-transcriptional level. Pre-treatment with CT-1 reduces the ability of heat shock to induce hsp expression and this effect occurs at the transcriptional level. Hence, CT-1 and stress induce the hsps via different pathways which can antagonise one another. The mechanisms of these effects and their potential impact on the use of CT-1 as a cardioprotective agent are discussed.