Role of a Unique Innovative Device (HEAR-O-SCOPE) in Prevention of Noise Induced Hearing Loss

Introduction Noise induced hearing loss has great significance in today’s world as it comes as an occupational health hazard accompanied with other systemic adverse effects like several neuropsychiatric disorders, cardiovascular diseases, or peptic ulcers. It can be prevented by serial follow up with pure tone audiograms and use of noise protectors like ear muffs or ear plugs. This article demonsrates an easy-to-adopt method of preventing noise induced hearing loss in the form of an electronic device named HEAR-O-SCOPE. Device Design This device is essentially a decibel meter which senses sound intensities above 85 decibel and equates it with permissible time of exposure for that decibel range and if permissible time of exposure is crossed, sends alarm signals in the form of buzzer and display, giving the user adequate time either to move away from the noisy surrounding or put in noise protectors. This device also has provision for real-time graphical plotting facilities. Expected Benefits Expected outcome by using this device in the long run would be early detection and prevention of noise induced hearing loss and other health hazards of noise pollution. Conclusion Regular use of HEAR-O-SCOPE is highly recommendable for prevention of Noise Induced Hearing Loss

Cannabinoid Receptor 2 (CB2) Plays a Role in the Generation of Germinal Center and Memory B Cells, but Not in the Production of Antigen-Specific IgG and IgM, in Response to T-dependent Antigens.

The cannabinoid receptor 2 (CB2) has been reported to modulate B cell functions including migration, proliferation and isotype class switching. Since these processes are required for the generation of the germinal center (GC) and antigen-specific plasma and memory cells following immunization with a T-dependent antigen, CB2 has the capacity to alter the quality and magnitude of T-dependent immune responses. To address this question, we immunized WT and CB2(-/-) mice with the T-dependent antigen 4-hydroxy-3-nitrophenylacetyl (NP)-chicken-gamma-globulin (CGG) and measured GC B cell formation and the generation of antigen-specific B cells and serum immunoglobulin (Ig). While there was a significant reduction in the number of splenic GC B cells in CB2(-/-) mice early in the response there was no detectable difference in the number of NP-specific IgM and IgG1 plasma cells. There was also no difference in NP-specific IgM and class switched IgG1 in the serum. In addition, we found no defect in the homing of plasma cells to the bone marrow (BM) and affinity maturation, although memory B cell cells in the spleen were reduced in CB2(-/-) mice. CB2-deficient mice also generated similar levels of antigen-specific IgM and IgG in the serum as WT following immunization with sheep red blood cells (sRBC). This study demonstrates that although CB2 plays a role in promoting GC and memory B cell formation/maintenance in the spleen, it is dispensable on all immune cell types required for the generation of antigen-specific IgM and IgG in T-dependent immune responses

GC B cells are reduced, but antigen-specific plasma B cell formation and antigen-specific serum IgM and IgG₁ levels are unaltered in CB2^−/− mice upon i.p.

<p>immunization with a T-dependent antigen. WT (open bars) and CB2^−/− (closed bars) mice were i.p. immunized with 30 µg alum-precipitated NP-CGG. (A–D) Spleens and BM were collected before (day 0) or 7, 11, 14, and 28 days after immunization for the analysis of GC B cells in the spleen by flow cytometry (A) and NP-specific IgM and IgG₁-secreting plasma cells in the spleen (B, C, respectively) and BM (D) by ELISPOT. (A) The percentage of Fas⁺GL7⁺ GC B cells within the B220⁺ population is shown. (B–D) Frequencies of NP-specific IgM⁺ (B) and IgG₁⁺ spots (C) per 10⁶ splenocytes and NP-specific IgG₁⁺ spots per 10⁶ BM cells (D) on the indicated days are shown. (E, F) Serum was collected from NP-CGG-immunized WT and CB2^−/− mice on days 0, 7, 14 and 28 and NP-specific IgM and IgG₁ titers were measured from two-fold serially diluted serum (1/400 to 1/3200 for IgM and 1/20000 to 1/160000 for IgG₁) by ELISA. The O.D. value for NP-specific IgM at the 1/1600 dilution (E) and NP-specific IgG₁ at the 1/40000 dilution (F) are shown. Data shown are the mean ± SEM from two independent experiments each with 3–4 mice per group. **p<0.01.</p

Upon s.c. immunization with NP-CGG GC formation occurs primarily in the draining LN.

<p>WT and CB2^−/− mice were s.c. immunized with 30 µg alum-precipitated NP-CGG s.c. on the shoulders. On day seven, the draining brachial and non-draining axillary LN and the spleen were collected and GC B cells were analyzed by flow cytometry. Representative dot plots show relative frequencies of Fas⁺GL7⁺ GC B cells within the B220⁺ population in the brachial LN (top row), axillary LN (middle row), and the spleen (bottom row) from unimmunized controls (left panels), immunized WT (middle panels) and CB2^−/− (right panels) mice. Numbers on the plots represent the percentage of cells in the corresponding gate. Data shown are one representative experiment of three.</p

CB2-deficiency does not affect affinity maturation.

<p>WT (open bars) and CB2^−/− (closed bars) mice were immunized with 30 µg NP-CGG in alum (i.p.) and rechallenged with 30 µg of NP-CGG in PBS (i.p.) on day 42 post-primary immunization. BM and serum were collected on day 28 after the primary and day seven after the secondary immunization for the analysis of affinity maturation. (A) Frequencies of high affinity (NP₄-specific) and total (NP₂₅-specific) antigen-specific IgG₁-secreting plasma cells per 10⁶ BM cells were determined by ELISPOT. Affinity maturation calculated as a ratio of high affinity to total antigen-specific IgG₁-secreting cells (NP₄:NP₂₅) is shown. (B) The titers of high affinity (NP₄-specific) and total (NP₂₅-specific) antigen-specific IgG₁ were determined from two-fold serially diluted serum (1/20000 to 1/160000) by ELISA and the O.D. values at the 1/40000 dilution were used to calculate affinity maturation. Affinity maturation calculated as an O.D. ratio of high affinity to total antigen-specific IgG₁ (NP₄:NP₂₅) is shown. Data shown are the mean ± SEM from two independent experiments each with 2–4 mice per group (n = 6–7).</p

What we know and do not know about the cannabinoid receptor 2 (CB2)

It well appreciated that the endocannabinoid system can regulate immune responses via the cannabinoid receptor 2 (CB2), which is primarily expressed by cells of the hematopoietic system. The endocannabinoid system is composed of receptors, ligands and enzymes controlling the synthesis and degradation of endocannabinoids. Along with endocannabinoids, both plant-derived and synthetic cannabinoids have been shown to bind to and signal through CB2 via G proteins leading to both inhibitory and stimulatory signals depending on the biological process. Because no cannabinoid ligand has been identified that only binds to CB2, the generation of mice deficient in CB2 has greatly expanded our knowledge of how CB2 contributes to immune cell development and function in health and disease. In regards to humans, genetic studies have associated CB2 with a variety of human diseases. Here, we review the endocannabinoid system with an emphasis on CB2 and its role in the immune system